make a presentation on covid 19

• Patient Care & Health Information
• Diseases & Conditions
• Coronavirus disease 2019 (COVID-19)

COVID-19, also called coronavirus disease 2019, is an illness caused by a virus. The virus is called severe acute respiratory syndrome coronavirus 2, or more commonly, SARS-CoV-2. It started spreading at the end of 2019 and became a pandemic disease in 2020.

• Coronavirus

Coronaviruses are a family of viruses. These viruses cause illnesses such as the common cold, severe acute respiratory syndrome (SARS), Middle East respiratory syndrome (MERS) and coronavirus disease 2019 (COVID-19).

The virus that causes COVID-19 spreads most commonly through the air in tiny droplets of fluid between people in close contact. Many people with COVID-19 have no symptoms or mild illness. But for older adults and people with certain medical conditions, COVID-19 can lead to the need for care in the hospital or death.

Staying up to date on your COVID-19 vaccine helps prevent serious illness, the need for hospital care due to COVID-19 and death from COVID-19 . Other ways that may help prevent the spread of this coronavirus includes good indoor air flow, physical distancing, wearing a mask in the right setting and good hygiene.

Medicine can limit the seriousness of the viral infection. Most people recover without long-term effects, but some people have symptoms that continue for months.

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Typical COVID-19 symptoms often show up 2 to 14 days after contact with the virus.

Symptoms can include:

• Shortness of breath.
• Loss of taste or smell.
• Extreme tiredness, called fatigue.
• Digestive symptoms such as upset stomach, vomiting or loose stools, called diarrhea.
• Pain, such as headaches and body or muscle aches.
• Fever or chills.
• Cold-like symptoms such as congestion, runny nose or sore throat.

People may only have a few symptoms or none. People who have no symptoms but test positive for COVID-19 are called asymptomatic. For example, many children who test positive don't have symptoms of COVID-19 illness. People who go on to have symptoms are considered presymptomatic. Both groups can still spread COVID-19 to others.

Some people may have symptoms that get worse about 7 to 14 days after symptoms start.

Most people with COVID-19 have mild to moderate symptoms. But COVID-19 can cause serious medical complications and lead to death. Older adults or people who already have medical conditions are at greater risk of serious illness.

COVID-19 may be a mild, moderate, severe or critical illness.

• In broad terms, mild COVID-19 doesn't affect the ability of the lungs to get oxygen to the body.
• In moderate COVID-19 illness, the lungs also work properly but there are signs that the infection is deep in the lungs.
• Severe COVID-19 means that the lungs don't work correctly, and the person needs oxygen and other medical help in the hospital.
• Critical COVID-19 illness means the lung and breathing system, called the respiratory system, has failed and there is damage throughout the body.

Rarely, people who catch the coronavirus can develop a group of symptoms linked to inflamed organs or tissues. The illness is called multisystem inflammatory syndrome. When children have this illness, it is called multisystem inflammatory syndrome in children, shortened to MIS -C. In adults, the name is MIS -A.

When to see a doctor

Contact a healthcare professional if you test positive for COVID-19 . If you have symptoms and need to test for COVID-19 , or you've been exposed to someone with COVID-19 , a healthcare professional can help.

People who are at high risk of serious illness may get medicine to block the spread of the COVID-19 virus in the body. Or your healthcare team may plan regular checks to monitor your health.

Get emergency help right away for any of these symptoms:

• Can't catch your breath or have problems breathing.
• Skin, lips or nail beds that are pale, gray or blue.
• New confusion.
• Trouble staying awake or waking up.
• Chest pain or pressure that is constant.

This list doesn't include every emergency symptom. If you or a person you're taking care of has symptoms that worry you, get help. Let the healthcare team know about a positive test for COVID-19 or symptoms of the illness.

More Information

• COVID-19 vs. flu: Similarities and differences
• COVID-19, cold, allergies and the flu
• Unusual symptoms of coronavirus

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COVID-19 is caused by infection with the severe acute respiratory syndrome coronavirus 2, also called SARS-CoV-2.

The coronavirus spreads mainly from person to person, even from someone who is infected but has no symptoms. When people with COVID-19 cough, sneeze, breathe, sing or talk, their breath may be infected with the COVID-19 virus.

The coronavirus carried by a person's breath can land directly on the face of a nearby person, after a sneeze or cough, for example. The droplets or particles the infected person breathes out could possibly be breathed in by other people if they are close together or in areas with low air flow. And a person may touch a surface that has respiratory droplets and then touch their face with hands that have the coronavirus on them.

It's possible to get COVID-19 more than once.

• Over time, the body's defense against the COVID-19 virus can fade.
• A person may be exposed to so much of the virus that it breaks through their immune defense.
• As a virus infects a group of people, the virus copies itself. During this process, the genetic code can randomly change in each copy. The changes are called mutations. If the coronavirus that causes COVID-19 changes in ways that make previous infections or vaccination less effective at preventing infection, people can get sick again.

The virus that causes COVID-19 can infect some pets. Cats, dogs, hamsters and ferrets have caught this coronavirus and had symptoms. It's rare for a person to get COVID-19 from a pet.

Risk factors

The main risk factors for COVID-19 are:

• If someone you live with has COVID-19 .
• If you spend time in places with poor air flow and a higher number of people when the virus is spreading.
• If you spend more than 30 minutes in close contact with someone who has COVID-19 .

Many factors affect your risk of catching the virus that causes COVID-19 . How long you are in contact, if the space has good air flow and your activities all affect the risk. Also, if you or others wear masks, if someone has COVID-19 symptoms and how close you are affects your risk. Close contact includes sitting and talking next to one another, for example, or sharing a car or bedroom.

It seems to be rare for people to catch the virus that causes COVID-19 from an infected surface. While the virus is shed in waste, called stool, COVID-19 infection from places such as a public bathroom is not common.

Serious COVID-19 illness risk factors

Some people are at a higher risk of serious COVID-19 illness than others. This includes people age 65 and older as well as babies younger than 6 months. Those age groups have the highest risk of needing hospital care for COVID-19 .

Not every risk factor for serious COVID-19 illness is known. People of all ages who have no other medical issues have needed hospital care for COVID-19 .

Known risk factors for serious illness include people who have not gotten a COVID-19 vaccine. Serious illness also is a higher risk for people who have:

• Sickle cell disease or thalassemia.
• Serious heart diseases and possibly high blood pressure.
• Chronic kidney, liver or lung diseases.

People with dementia or Alzheimer's also are at higher risk, as are people with brain and nervous system conditions such as stroke. Smoking increases the risk of serious COVID-19 illness. And people with a body mass index in the overweight category or obese category may have a higher risk as well.

Other medical conditions that may raise the risk of serious illness from COVID-19 include:

• Cancer or a history of cancer.
• Type 1 or type 2 diabetes.
• Weakened immune system from solid organ transplants or bone marrow transplants, some medicines, or HIV .

This list is not complete. Factors linked to a health issue may raise the risk of serious COVID-19 illness too. Examples are a medical condition where people live in a group home, or lack of access to medical care. Also, people with more than one health issue, or people of older age who also have health issues have a higher chance of severe illness.

Related information

• COVID-19: Who's at higher risk of serious symptoms? - Related information COVID-19: Who's at higher risk of serious symptoms?

Complications

Complications of COVID-19 include long-term loss of taste and smell, skin rashes, and sores. The illness can cause trouble breathing or pneumonia. Medical issues a person already manages may get worse.

Complications of severe COVID-19 illness can include:

• Acute respiratory distress syndrome, when the body's organs do not get enough oxygen.
• Shock caused by the infection or heart problems.
• Overreaction of the immune system, called the inflammatory response.
• Blood clots.
• Kidney injury.

Post-COVID-19 syndrome

After a COVID-19 infection, some people report that symptoms continue for months, or they develop new symptoms. This syndrome has often been called long COVID, or post- COVID-19 . You might hear it called long haul COVID-19 , post-COVID conditions or PASC. That's short for post-acute sequelae of SARS -CoV-2.

Other infections, such as the flu and polio, can lead to long-term illness. But the virus that causes COVID-19 has only been studied since it began to spread in 2019. So, research into the specific effects of long-term COVID-19 symptoms continues.

Researchers do think that post- COVID-19 syndrome can happen after an illness of any severity.

Getting a COVID-19 vaccine may help prevent post- COVID-19 syndrome.

• Long-term effects of COVID-19

The Centers for Disease Control and Prevention (CDC) recommends a COVID-19 vaccine for everyone age 6 months and older. The COVID-19 vaccine can lower the risk of death or serious illness caused by COVID-19. It lowers your risk and lowers the risk that you may spread it to people around you.

The COVID-19 vaccines available in the United States are:

2023-2024 Pfizer-BioNTech COVID-19 vaccine. This vaccine is available for people age 6 months and older.

Among people with a typical immune system:

• Children age 6 months up to age 4 years are up to date after three doses of a Pfizer-BioNTech COVID-19 vaccine.
• People age 5 and older are up to date after one Pfizer-BioNTech COVID-19 vaccine.
• For people who have not had a 2023-2024 COVID-19 vaccination, the CDC recommends getting an additional shot of that updated vaccine.

2023-2024 Moderna COVID-19 vaccine. This vaccine is available for people age 6 months and older.

• Children ages 6 months up to age 4 are up to date if they've had two doses of a Moderna COVID-19 vaccine.
• People age 5 and older are up to date with one Moderna COVID-19 vaccine.

2023-2024 Novavax COVID-19 vaccine. This vaccine is available for people age 12 years and older.

• People age 12 years and older are up to date if they've had two doses of a Novavax COVID-19 vaccine.

In general, people age 5 and older with typical immune systems can get any vaccine approved or authorized for their age. They usually don't need to get the same vaccine each time.

Some people should get all their vaccine doses from the same vaccine maker, including:

• Children ages 6 months to 4 years.
• People age 5 years and older with weakened immune systems.
• People age 12 and older who have had one shot of the Novavax vaccine should get the second Novavax shot in the two-dose series.

Talk to your healthcare professional if you have any questions about the vaccines for you or your child. Your healthcare team can help you if:

• The vaccine you or your child got earlier isn't available.
• You don't know which vaccine you or your child received.
• You or your child started a vaccine series but couldn't finish it due to side effects.

People with weakened immune systems

Your health care team may suggest added doses of COVID-19 vaccine if you have a moderately or severely weakened immune system.

Control the spread of infection

In addition to vaccination, there are other ways to stop the spread of the virus that causes COVID-19 .

If you are at a higher risk of serious illness, talk to your healthcare professional about how best to protect yourself. Know what to do if you get sick so you can quickly start treatment.

If you feel ill or have COVID-19 , stay home and away from others, including pets, if possible. Avoid sharing household items such as dishes or towels if you're sick.

In general, make it a habit to:

• Test for COVID-19 . If you have symptoms of COVID-19 test for the infection. Or test five days after you came in contact with the virus.
• Help from afar. Avoid close contact with anyone who is sick or has symptoms, if possible.
• Wash your hands. Wash your hands well and often with soap and water for at least 20 seconds. Or use an alcohol-based hand sanitizer with at least 60% alcohol.
• Cover your coughs and sneezes. Cough or sneeze into a tissue or your elbow. Then wash your hands.
• Clean and disinfect high-touch surfaces. For example, clean doorknobs, light switches, electronics and counters regularly.

Try to spread out in crowded public areas, especially in places with poor airflow. This is important if you have a higher risk of serious illness.

The CDC recommends that people wear a mask in indoor public spaces if you're in an area with a high number of people with COVID-19 in the hospital. They suggest wearing the most protective mask possible that you'll wear regularly, that fits well and is comfortable.

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Travel and COVID-19

Travel brings people together from areas where illnesses may be at higher levels. Masks can help slow the spread of respiratory diseases in general, including COVID-19 . Masks help the most in places with low air flow and where you are in close contact with other people. Also, masks can help if the places you travel to or through have a high level of illness.

Masking is especially important if you or a companion have a high risk of serious illness from COVID-19 .

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• Goldman L, et al., eds. COVID-19: Epidemiology, clinical manifestations, diagnosis, community prevention, and prognosis. In: Goldman-Cecil Medicine. 27th ed. Elsevier; 2024. https://www.clinicalkey.com. Accessed Dec. 17, 2023.
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• Interim clinical considerations for use of COVID-19 vaccines currently approved or authorized in the United States. Centers for Disease Control and Prevention. https://www.cdc.gov/vaccines/covid-19/clinical-considerations/covid-19-vaccines-us.html#CoV-19-vaccination. Accessed Jan. 10, 2024.
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• How to protect yourself and others. Centers for Disease Control and Prevention. https://www.cdc.gov/coronavirus/2019-ncov/prevent-getting-sick/prevention.html. Accessed Jan. 10, 2024.
• People who are immunocompromised. Centers for Disease Control and Prevention. https://www.cdc.gov/coronavirus/2019-ncov/need-extra-precautions/people-who-are-immunocompromised.html. Accessed Jan. 10, 2024.
• Masking during travel. Centers for Disease Control and Prevention. https://wwwnc.cdc.gov/travel/page/masks. Accessed Jan. 10, 2024.
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• COVID-19 test basics. U.S. Food and Drug Administration. https://www.fda.gov/consumers/consumer-updates/covid-19-test-basics. Accessed Jan. 11, 2024.
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Clinical presentation and course of COVID-19

Affiliations.

• 1 Department of Infectious Disease, Respiratory Institute, Cleveland Clinic.
• 2 Vice-Chair, Department of Infectious Disease, Respiratory Institute, Cleveland Clinic; Assistant Professor, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH [email protected].
• PMID: 32371564
• DOI: 10.3949/ccjm.87a.ccc013

Information about the clinical presentation and course of COVID-19 is evolving rapidly. On presentation, cough and fever predominate, but extrapulmonary symptoms are also common; in some patients, loss of sense of smell may be an early but favorable sign. The mortality rate varies widely in different reports but should become clearer as more data are collected. Risk factors for severe disease and death include comorbid conditions such as hypertension, cardiovascular disease, diabetes mellitus, and chronic obstructive pulmonary disease. Other implicated factors include older age, obesity, end-stage renal disease, and a higher neutrophil-lymphocyte ratio.

Copyright © 2020 The Cleveland Clinic Foundation. All Rights Reserved.

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• Clinical Deterioration
• Comorbidity
• Coronavirus Infections / diagnosis
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• Survival Analysis
• Symptom Assessment / methods*
• Symptom Assessment / statistics & numerical data

Masks and Respiratory Viruses Prevention

Wearing a mask is an additional prevention strategy that you can choose to further protect yourself and others.

An additional strategy to further protect yourself and others

How it works

Generally, masks can help act as a filter to reduce the number of germs you breathe in or out. Their effectiveness can vary against different viruses, for example, based on the size of the virus. When worn by a person who has a virus, masks can reduce the chances they spread it to others. Masks can also protect wearers from inhaling germs; this type of protection typically comes from better fitting masks (for example, N95 or KN95 respirators).

There are many different types of masks  that have varying abilities to block viruses depending on their design and how well they fit against your face. Cloth masks generally offer lower levels of protection to wearers, surgical/disposable masks usually offer more protection, international filtering facepiece respirators (like KN95 respirators) offer even more, and the most protective respirators are NIOSH Approved® filtering facepiece respirators (like N95® respirators).

Steps you can take

Individuals can

• When choosing to wear a mask, choose the most protective type you can. Determine how well it fits. Gaps can let air leak in and out. Check for gaps by cupping your hands around the outside edges of the mask. If the mask has a good fit, you will feel warm air come through the front of the mask and may be able to see the mask material move in and out with each breath.
• Learn about proper technique  for wearing an N95 respirator.

Organizations can

• Provide free, high-quality masks to your workforce or visitors in times of higher respiratory viral spread.

Key times for prevention

All of the prevention strategies described in this guidance can be helpful to reduce risk. They are especially helpful when:

• Respiratory viruses are causing a lot of  illness in your community .
• You or the people around you were recently exposed to a respiratory virus, are sick, or are recovering
• You or the people around you have  risk factors for severe illness .

CDC offers separate, specific guidance for healthcare settings ( COVID-19 , flu , and  general infection prevention and control ).  Federal civil rights laws  may require reasonable modifications or reasonable accommodations in various circumstances. Nothing in this guidance is intended to detract from or supersede those laws.

• Preventing Respiratory Viruses
• Hygiene and Respiratory Viruses Prevention
• Taking Steps for Cleaner Air for Respiratory Virus Prevention
• Preventing Spread of Respiratory Viruses When You’re Sick
• About Physical Distancing and Respiratory Viruses
• Testing and Respiratory Viruses

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AI tool predicts COVID-19 vaccine uptake

• Global Health

Findings of a new study led by researchers at Northwestern University and the University of Cincinnati could help public health officials lead more effective vaccination campaigns that overcome hesitancy.

The research team of computer scientists, psychiatrists and social scientists, created a predictive model using a powerful combination of machine learning algorithms and cognitive science. The novel interpretation method, coined “Comp Cog AI” by the team, uses small variable sets as opposed to the big data traditionally associated with AI.

The paper was published March 18 in the Journal of Medical Internet Research .

“While the importance of medical factors has played a large role in public health research, there is an emerging recognition that behavioral and emotional factors are just as important,” said co-senior author Aggelos Katsaggelos . “In our research, we see that understanding an individual’s behavioral factors may be useful in targeted vaccination initiatives such as during a pandemic.”

Katsaggelos is the Joseph Cummings Professor of Electrical and Computer Engineering at Northwestern’s McCormick School of Engineering and director of the Image and Video Processing Lab at Northwestern.

Researchers surveyed 3,476 adults across the United States in 2021 during the COVID-19 pandemic. At the time of the survey, the first vaccine by Pfizer had been available for more than a year.

Respondents provided information about their demographics such as where they live, income, highest education level completed, ethnicity and access to the internet. The respondents’ demographics mirrored those of the United States based on U.S. Census Bureau figures.

Participants were asked if they had received either of the available COVID-19 vaccines. About 73% of respondents said they were vaccinated, slightly more than the 70% of the nation's population that had been vaccinated in 2021.

Further, they were asked if they routinely followed four precautionary suggestions designed to prevent the spread of the virus: wearing a mask, social distancing, washing their hands and not gathering in large groups.

Patients were then asked to rank a random sequence of 48 pictures on a seven-point like-to-dislike scale of 3 to -3 in six categories: sports, disasters, cute animals, aggressive animals, nature and food.

Hans Breiter, a psychiatrist at the University of Cincinnati, said the goal of this exercise is to establish a unique snapshot of each respondent’s judgments. These variables include concepts familiar to behavioral economists — or people who gamble — such as aversion to risk or loss or the point at which someone is willing to expose themselves to risk for a reward or else forfeit that reward to avoid risk.

“The framework for our judgment is important,” Breiter said. “It gets at how we make choices about medical decisions.”

The judgment variables and demographics were compared between respondents who were vaccinated and those who were not. Three machine learning approaches were used to test how well the respondents’ judgement, demographics and attitudes toward COVID-19 precautions predicted vaccine uptake.

“Our research may be of interest to policymakers and healthcare professionals for designing efficient campaigns that focus on individuals most likely to respond to vaccination suggestions,” said co-second author and Northwestern Ph.D. student Shamal Lalvani.

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New data show Paxlovid outperforms molnupiravir against severe COVID-19 outcomes

Staff photo by Jim Wappes

A large study yesterday in the International Journal of Infectious Diseases shows that, if prescribed within 5 days of confirmed infection, Paxlovid (nirmatrelvir-ritonavir) is more effective in protecting against all-cause mortality and severe COVID-19 in adults than is molnupiravir, another antiviral drug.

The study was conducted in Hong Kong in 2022. Researchers said they also found no significant difference between CoronaVac (made by Sinovac Biotech) and Comirnaty (Pfizer-BioNTech) vaccines in the effectiveness of reducing all-cause mortality and progression to severe COVID-19.

The authors of the study assessed 61,105 hospitalized adult patients in Hong Kong who had confirmed SARS-CoV-2 infection from March 16 to December 31, 2022. During the study period, Omicron BA.2 and BA.5 subvariants were dominant.

The primary outcome was all-cause 28-day mortality from a confirmed COVID-19 infection. A secondary outcome was the development of severe illness, defined as requiring intubation, intensive care unit admission, extracorporeal membrane oxygenation, shock, or oxygen supplement of at least three liters per minute.

A total of 16,068 (26.3%) of patients were treated with molnupiravir, and 18,113 (29.6%) were treated with Paxlovid. About 44% of patients did not receive antiviral treatments.

Efficacy depends on early treatment

The molnupiravir users, Paxlovid users, and controls had cumulative fatal incidences of 1,404, 245, and 2,732, respectively, and severe case incidences of 1,766, 794, and 2,848, respectively.

Paxlovid use within 5 days of confirmed infection for those 18 to 59 years was associated with a significantly lower risk of all-cause mortality (hazard ratio [HR], 0.48; 95% confidence interval, 0.25 to 0.92).

Molnupiravir was also associated with significantly lower risks of all-cause mortality and progression to severe COVID-19 for patients aged 60 to 79 years (mortality and severe case HRs of 0.65 and 0.69, respectively).

"Given prescriptions were made within five days of confirmed infection, the use of nirmatrelvir-ritonavir was associated significantly lower risks of all-cause mortality and progression to severe COVID-19 than those of molnupiravir across all three age groups," the authors wrote. The third age-group assessed was people 80 and older.

The use of nirmatrelvir-ritonavir was associated significantly lower risks of all-cause mortality and progression to severe COVID-19 than those of molnupiravir.

No significant benefit was found for oral antivirals prescribed beyond 5 days of confirmed infection, the authors said. Both Comirnaty and CoronaVac were found to be equally effective in preventing severe outcomes, in all age-groups.

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Four of the biggest problems facing education—and four trends that could make a difference

Eduardo velez bustillo, harry a. patrinos.

In 2022, we published, Lessons for the education sector from the COVID-19 pandemic , which was a follow up to,  Four Education Trends that Countries Everywhere Should Know About , which summarized views of education experts around the world on how to handle the most pressing issues facing the education sector then. We focused on neuroscience, the role of the private sector, education technology, inequality, and pedagogy.

Unfortunately, we think the four biggest problems facing education today in developing countries are the same ones we have identified in the last decades .

1. The learning crisis was made worse by COVID-19 school closures

Low quality instruction is a major constraint and prior to COVID-19, the learning poverty rate in low- and middle-income countries was 57% (6 out of 10 children could not read and understand basic texts by age 10). More dramatic is the case of Sub-Saharan Africa with a rate even higher at 86%. Several analyses show that the impact of the pandemic on student learning was significant, leaving students in low- and middle-income countries way behind in mathematics, reading and other subjects.  Some argue that learning poverty may be close to 70% after the pandemic , with a substantial long-term negative effect in future earnings. This generation could lose around $21 trillion in future salaries, with the vulnerable students affected the most.

2. Countries are not paying enough attention to early childhood care and education (ECCE)

At the pre-school level about two-thirds of countries do not have a proper legal framework to provide free and compulsory pre-primary education. According to UNESCO, only a minority of countries, mostly high-income, were making timely progress towards SDG4 benchmarks on early childhood indicators prior to the onset of COVID-19. And remember that ECCE is not only preparation for primary school. It can be the foundation for emotional wellbeing and learning throughout life; one of the best investments a country can make.

3. There is an inadequate supply of high-quality teachers

Low quality teaching is a huge problem and getting worse in many low- and middle-income countries.  In Sub-Saharan Africa, for example, the percentage of trained teachers fell from 84% in 2000 to 69% in 2019 . In addition, in many countries teachers are formally trained and as such qualified, but do not have the minimum pedagogical training. Globally, teachers for science, technology, engineering, and mathematics (STEM) subjects are the biggest shortfalls.

4. Decision-makers are not implementing evidence-based or pro-equity policies that guarantee solid foundations

It is difficult to understand the continued focus on non-evidence-based policies when there is so much that we know now about what works. Two factors contribute to this problem. One is the short tenure that top officials have when leading education systems. Examples of countries where ministers last less than one year on average are plentiful. The second and more worrisome deals with the fact that there is little attention given to empirical evidence when designing education policies.

To help improve on these four fronts, we see four supporting trends:

1. Neuroscience should be integrated into education policies

Policies considering neuroscience can help ensure that students get proper attention early to support brain development in the first 2-3 years of life. It can also help ensure that children learn to read at the proper age so that they will be able to acquire foundational skills to learn during the primary education cycle and from there on. Inputs like micronutrients, early child stimulation for gross and fine motor skills, speech and language and playing with other children before the age of three are cost-effective ways to get proper development. Early grade reading, using the pedagogical suggestion by the Early Grade Reading Assessment model, has improved learning outcomes in many low- and middle-income countries. We now have the tools to incorporate these advances into the teaching and learning system with AI , ChatGPT , MOOCs and online tutoring.

2. Reversing learning losses at home and at school

There is a real need to address the remaining and lingering losses due to school closures because of COVID-19.  Most students living in households with incomes under the poverty line in the developing world, roughly the bottom 80% in low-income countries and the bottom 50% in middle-income countries, do not have the minimum conditions to learn at home . These students do not have access to the internet, and, often, their parents or guardians do not have the necessary schooling level or the time to help them in their learning process. Connectivity for poor households is a priority. But learning continuity also requires the presence of an adult as a facilitator—a parent, guardian, instructor, or community worker assisting the student during the learning process while schools are closed or e-learning is used.

To recover from the negative impact of the pandemic, the school system will need to develop at the student level: (i) active and reflective learning; (ii) analytical and applied skills; (iii) strong self-esteem; (iv) attitudes supportive of cooperation and solidarity; and (v) a good knowledge of the curriculum areas. At the teacher (instructor, facilitator, parent) level, the system should aim to develop a new disposition toward the role of teacher as a guide and facilitator. And finally, the system also needs to increase parental involvement in the education of their children and be active part in the solution of the children’s problems. The Escuela Nueva Learning Circles or the Pratham Teaching at the Right Level (TaRL) are models that can be used.

3. Use of evidence to improve teaching and learning

We now know more about what works at scale to address the learning crisis. To help countries improve teaching and learning and make teaching an attractive profession, based on available empirical world-wide evidence , we need to improve its status, compensation policies and career progression structures; ensure pre-service education includes a strong practicum component so teachers are well equipped to transition and perform effectively in the classroom; and provide high-quality in-service professional development to ensure they keep teaching in an effective way. We also have the tools to address learning issues cost-effectively. The returns to schooling are high and increasing post-pandemic. But we also have the cost-benefit tools to make good decisions, and these suggest that structured pedagogy, teaching according to learning levels (with and without technology use) are proven effective and cost-effective .

4. The role of the private sector

When properly regulated the private sector can be an effective education provider, and it can help address the specific needs of countries. Most of the pedagogical models that have received international recognition come from the private sector. For example, the recipients of the Yidan Prize on education development are from the non-state sector experiences (Escuela Nueva, BRAC, edX, Pratham, CAMFED and New Education Initiative). In the context of the Artificial Intelligence movement, most of the tools that will revolutionize teaching and learning come from the private sector (i.e., big data, machine learning, electronic pedagogies like OER-Open Educational Resources, MOOCs, etc.). Around the world education technology start-ups are developing AI tools that may have a good potential to help improve quality of education .

After decades asking the same questions on how to improve the education systems of countries, we, finally, are finding answers that are very promising.  Governments need to be aware of this fact.

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Consultant, Education Sector, World Bank

Senior Adviser, Education

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• The role of COVID-19 vaccines in preventing post-COVID-19 thromboembolic and cardiovascular complications
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• Núria Mercadé-Besora 1 , 2 , 3 ,
• Xintong Li 1 ,
• Raivo Kolde 4 ,
• Nhung TH Trinh 5 ,
• Maria T Sanchez-Santos 1 ,
• Wai Yi Man 1 ,
• Elena Roel 3 ,
• Carlen Reyes 3 ,
• http://orcid.org/0000-0003-0388-3403 Antonella Delmestri 1 ,
• Hedvig M E Nordeng 6 , 7 ,
• http://orcid.org/0000-0002-4036-3856 Anneli Uusküla 8 ,
• http://orcid.org/0000-0002-8274-0357 Talita Duarte-Salles 3 , 9 ,
• Clara Prats 2 ,
• http://orcid.org/0000-0002-3950-6346 Daniel Prieto-Alhambra 1 , 9 ,
• http://orcid.org/0000-0002-0000-0110 Annika M Jödicke 1 ,
• Martí Català 1
• 1 Pharmaco- and Device Epidemiology Group, Health Data Sciences, Botnar Research Centre, NDORMS , University of Oxford , Oxford , UK
• 2 Department of Physics , Universitat Politècnica de Catalunya , Barcelona , Spain
• 3 Fundació Institut Universitari per a la recerca a l'Atenció Primària de Salut Jordi Gol i Gurina (IDIAPJGol) , IDIAP Jordi Gol , Barcelona , Catalunya , Spain
• 4 Institute of Computer Science , University of Tartu , Tartu , Estonia
• 5 Pharmacoepidemiology and Drug Safety Research Group, Department of Pharmacy, Faculty of Mathematics and Natural Sciences , University of Oslo , Oslo , Norway
• 6 School of Pharmacy , University of Oslo , Oslo , Norway
• 7 Division of Mental Health , Norwegian Institute of Public Health , Oslo , Norway
• 8 Department of Family Medicine and Public Health , University of Tartu , Tartu , Estonia
• 9 Department of Medical Informatics, Erasmus University Medical Center , Erasmus University Rotterdam , Rotterdam , Zuid-Holland , Netherlands
• Correspondence to Prof Daniel Prieto-Alhambra, Pharmaco- and Device Epidemiology Group, Health Data Sciences, Botnar Research Centre, NDORMS, University of Oxford, Oxford, UK; daniel.prietoalhambra{at}ndorms.ox.ac.uk

Objective To study the association between COVID-19 vaccination and the risk of post-COVID-19 cardiac and thromboembolic complications.

Methods We conducted a staggered cohort study based on national vaccination campaigns using electronic health records from the UK, Spain and Estonia. Vaccine rollout was grouped into four stages with predefined enrolment periods. Each stage included all individuals eligible for vaccination, with no previous SARS-CoV-2 infection or COVID-19 vaccine at the start date. Vaccination status was used as a time-varying exposure. Outcomes included heart failure (HF), venous thromboembolism (VTE) and arterial thrombosis/thromboembolism (ATE) recorded in four time windows after SARS-CoV-2 infection: 0–30, 31–90, 91–180 and 181–365 days. Propensity score overlap weighting and empirical calibration were used to minimise observed and unobserved confounding, respectively.

Fine-Gray models estimated subdistribution hazard ratios (sHR). Random effect meta-analyses were conducted across staggered cohorts and databases.

Results The study included 10.17 million vaccinated and 10.39 million unvaccinated people. Vaccination was associated with reduced risks of acute (30-day) and post-acute COVID-19 VTE, ATE and HF: for example, meta-analytic sHR of 0.22 (95% CI 0.17 to 0.29), 0.53 (0.44 to 0.63) and 0.45 (0.38 to 0.53), respectively, for 0–30 days after SARS-CoV-2 infection, while in the 91–180 days sHR were 0.53 (0.40 to 0.70), 0.72 (0.58 to 0.88) and 0.61 (0.51 to 0.73), respectively.

Conclusions COVID-19 vaccination reduced the risk of post-COVID-19 cardiac and thromboembolic outcomes. These effects were more pronounced for acute COVID-19 outcomes, consistent with known reductions in disease severity following breakthrough versus unvaccinated SARS-CoV-2 infection.

• Epidemiology
• PUBLIC HEALTH
• Electronic Health Records

Data availability statement

Data may be obtained from a third party and are not publicly available. CPRD: CPRD data were obtained under the CPRD multi-study license held by the University of Oxford after Research Data Governance (RDG) approval. Direct data sharing is not allowed. SIDIAP: In accordance with current European and national law, the data used in this study is only available for the researchers participating in this study. Thus, we are not allowed to distribute or make publicly available the data to other parties. However, researchers from public institutions can request data from SIDIAP if they comply with certain requirements. Further information is available online ( https://www.sidiap.org/index.php/menu-solicitudesen/application-proccedure ) or by contacting SIDIAP ([email protected]). CORIVA: CORIVA data were obtained under the approval of Research Ethics Committee of the University of Tartu and the patient level data sharing is not allowed. All analyses in this study were conducted in a federated manner, where analytical code and aggregated (anonymised) results were shared, but no patient-level data was transferred across the collaborating institutions.

This is an open access article distributed in accordance with the Creative Commons Attribution 4.0 Unported (CC BY 4.0) license, which permits others to copy, redistribute, remix, transform and build upon this work for any purpose, provided the original work is properly cited, a link to the licence is given, and indication of whether changes were made. See:  https://creativecommons.org/licenses/by/4.0/ .

https://doi.org/10.1136/heartjnl-2023-323483

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WHAT IS ALREADY KNOWN ON THIS TOPIC

COVID-19 vaccines proved to be highly effective in reducing the severity of acute SARS-CoV-2 infection.

While COVID-19 vaccines were associated with increased risk for cardiac and thromboembolic events, such as myocarditis and thrombosis, the risk of complications was substantially higher due to SARS-CoV-2 infection.

WHAT THIS STUDY ADDS

COVID-19 vaccination reduced the risk of heart failure, venous thromboembolism and arterial thrombosis/thromboembolism in the acute (30 days) and post-acute (31 to 365 days) phase following SARS-CoV-2 infection. This effect was stronger in the acute phase.

The overall additive effect of vaccination on the risk of post-vaccine and/or post-COVID thromboembolic and cardiac events needs further research.

HOW THIS STUDY MIGHT AFFECT RESEARCH, PRACTICE OR POLICY

COVID-19 vaccines proved to be highly effective in reducing the risk of post-COVID cardiovascular and thromboembolic complications.

Introduction

COVID-19 vaccines were approved under emergency authorisation in December 2020 and showed high effectiveness against SARS-CoV-2 infection, COVID-19-related hospitalisation and death. 1 2 However, concerns were raised after spontaneous reports of unusual thromboembolic events following adenovirus-based COVID-19 vaccines, an association that was further assessed in observational studies. 3 4 More recently, mRNA-based vaccines were found to be associated with a risk of rare myocarditis events. 5 6

On the other hand, SARS-CoV-2 infection can trigger cardiac and thromboembolic complications. 7 8 Previous studies showed that, while slowly decreasing over time, the risk for serious complications remain high for up to a year after infection. 9 10 Although acute and post-acute cardiac and thromboembolic complications following COVID-19 are rare, they present a substantial burden to the affected patients, and the absolute number of cases globally could become substantial.

Recent studies suggest that COVID-19 vaccination could protect against cardiac and thromboembolic complications attributable to COVID-19. 11 12 However, most studies did not include long-term complications and were conducted among specific populations.

Evidence is still scarce as to whether the combined effects of COVID-19 vaccines protecting against SARS-CoV-2 infection and reducing post-COVID-19 cardiac and thromboembolic outcomes, outweigh any risks of these complications potentially associated with vaccination.

We therefore used large, representative data sources from three European countries to assess the overall effect of COVID-19 vaccines on the risk of acute and post-acute COVID-19 complications including venous thromboembolism (VTE), arterial thrombosis/thromboembolism (ATE) and other cardiac events. Additionally, we studied the comparative effects of ChAdOx1 versus BNT162b2 on the risk of these same outcomes.

Data sources

We used four routinely collected population-based healthcare datasets from three European countries: the UK, Spain and Estonia.

For the UK, we used data from two primary care databases—namely, Clinical Practice Research Datalink, CPRD Aurum 13 and CPRD Gold. 14 CPRD Aurum currently covers 13 million people from predominantly English practices, while CPRD Gold comprises 3.1 million active participants mostly from GP practices in Wales and Scotland. Spanish data were provided by the Information System for the Development of Research in Primary Care (SIDIAP), 15 which encompasses primary care records from 6 million active patients (around 75% of the population in the region of Catalonia) linked to hospital admissions data (Conjunt Mínim Bàsic de Dades d’Alta Hospitalària). Finally, the CORIVA dataset based on national health claims data from Estonia was used. It contains all COVID-19 cases from the first year of the pandemic and ~440 000 randomly selected controls. CORIVA was linked to the death registry and all COVID-19 testing from the national health information system.

Databases included sociodemographic information, diagnoses, measurements, prescriptions and secondary care referrals and were linked to vaccine registries, including records of all administered vaccines from all healthcare settings. Data availability for CPRD Gold ended in December 2021, CPRD Aurum in January 2022, SIDIAP in June 2022 and CORIVA in December 2022.

All databases were mapped to the Observational Medical Outcomes Partnership Common Data Model (OMOP CDM) 16 to facilitate federated analytics.

Multinational network staggered cohort study: study design and participants

The study design has been published in detail elsewhere. 17 Briefly, we used a staggered cohort design considering vaccination as a time-varying exposure. Four staggered cohorts were designed with each cohort representing a country-specific vaccination rollout phase (eg, dates when people became eligible for vaccination, and eligibility criteria).

The source population comprised all adults registered in the respective database for at least 180 days at the start of the study (4 January 2021 for CPRD Gold and Aurum, 20 February 2021 for SIDIAP and 28 January 2021 for CORIVA). Subsequently, each staggered cohort corresponded to an enrolment period: all people eligible for vaccination during this time were included in the cohort and people with a history of SARS-CoV-2 infection or COVID-19 vaccination before the start of the enrolment period were excluded. Across countries, cohort 1 comprised older age groups, whereas cohort 2 comprised individuals at risk for severe COVID-19. Cohort 3 included people aged ≥40 and cohort 4 enrolled people aged ≥18.

In each cohort, people receiving a first vaccine dose during the enrolment period were allocated to the vaccinated group, with their index date being the date of vaccination. Individuals who did not receive a vaccine dose comprised the unvaccinated group and their index date was assigned within the enrolment period, based on the distribution of index dates in the vaccinated group. People with COVID-19 before the index date were excluded.

Follow-up started from the index date until the earliest of end of available data, death, change in exposure status (first vaccine dose for those unvaccinated) or outcome of interest.

COVID-19 vaccination

All vaccines approved within the study period from January 2021 to July 2021—namely, ChAdOx1 (Oxford/AstraZeneca), BNT162b2 (BioNTech/Pfizer]) Ad26.COV2.S (Janssen) and mRNA-1273 (Moderna), were included for this study.

Post-COVID-19 outcomes of interest

Outcomes of interest were defined as SARS-CoV-2 infection followed by a predefined thromboembolic or cardiac event of interest within a year after infection, and with no record of the same clinical event in the 6 months before COVID-19. Outcome date was set as the corresponding SARS-CoV-2 infection date.

COVID-19 was identified from either a positive SARS-CoV-2 test (polymerase chain reaction (PCR) or antigen), or a clinical COVID-19 diagnosis, with no record of COVID-19 in the previous 6 weeks. This wash-out period was imposed to exclude re-recordings of the same COVID-19 episode.

Post-COVID-19 outcome events were selected based on previous studies. 11–13 Events comprised ischaemic stroke (IS), haemorrhagic stroke (HS), transient ischaemic attack (TIA), ventricular arrhythmia/cardiac arrest (VACA), myocarditis/pericarditis (MP), myocardial infarction (MI), heart failure (HF), pulmonary embolism (PE) and deep vein thrombosis (DVT). We used two composite outcomes: (1) VTE, as an aggregate of PE and DVT and (2) ATE, as a composite of IS, TIA and MI. To avoid re-recording of the same complication we imposed a wash-out period of 90 days between records. Phenotypes for these complications were based on previously published studies. 3 4 8 18

All outcomes were ascertained in four different time periods following SARS-CoV-2 infection: the first period described the acute infection phase—that is, 0–30 days after COVID-19, whereas the later periods - which are 31–90 days, 91–180 days and 181–365 days, illustrate the post-acute phase ( figure 1 ).

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Study outcome design. Study outcomes of interest are defined as a COVID-19 infection followed by one of the complications in the figure, within a year after infection. Outcomes were ascertained in four different time windows after SARS-CoV-2 infection: 0–30 days (namely the acute phase), 31–90 days, 91–180 days and 181–365 days (these last three comprise the post-acute phase).

Negative control outcomes

Negative control outcomes (NCOs) were used to detect residual confounding. NCOs are outcomes which are not believed to be causally associated with the exposure, but share the same bias structure with the exposure and outcome of interest. Therefore, no significant association between exposure and NCO is to be expected. Our study used 43 different NCOs from previous work assessing vaccine effectiveness. 19

Statistical analysis

Federated network analyses.

A template for an analytical script was developed and subsequently tailored to include the country-specific aspects (eg, dates, priority groups) for the vaccination rollout. Analyses were conducted locally for each database. Only aggregated data were shared and person counts <5 were clouded.

Propensity score weighting

Large-scale propensity scores (PS) were calculated to estimate the likelihood of a person receiving the vaccine based on their demographic and health-related characteristics (eg, conditions, medications) prior to the index date. PS were then used to minimise observed confounding by creating a weighted population (overlap weighting 20 ), in which individuals contributed with a different weight based on their PS and vaccination status.

Prespecified key variables included in the PS comprised age, sex, location, index date, prior observation time in the database, number of previous outpatient visits and previous SARS-CoV-2 PCR/antigen tests. Regional vaccination, testing and COVID-19 incidence rates were also forced into the PS equation for the UK databases 21 and SIDIAP. 22 In addition, least absolute shrinkage and selection operator (LASSO) regression, a technique for variable selection, was used to identify additional variables from all recorded conditions and prescriptions within 0–30 days, 31–180 days and 181-any time (conditions only) before the index date that had a prevalence of >0.5% in the study population.

PS were then separately estimated for each staggered cohort and analysis. We considered covariate balance to be achieved if absolute standardised mean differences (ASMDs) were ≤0.1 after weighting. Baseline characteristics such as demographics and comorbidities were reported.

Effect estimation

To account for the competing risk of death associated with COVID-19, Fine-and-Grey models 23 were used to calculate subdistribution hazard ratios (sHRs). Subsequently, sHRs and confidence intervals were empirically calibrated from NCO estimates 24 to account for unmeasured confounding. To calibrate the estimates, the empirical null distribution was derived from NCO estimates and was used to compute calibrated confidence intervals. For each outcome, sHRs from the four staggered cohorts were pooled using random-effect meta-analysis, both separately for each database and across all four databases.

Sensitivity analysis

Sensitivity analyses comprised 1) censoring follow-up for vaccinated people at the time when they received their second vaccine dose and 2) considering only the first post-COVID-19 outcome within the year after infection ( online supplemental figure S1 ). In addition, comparative effectiveness analyses were conducted for BNT162b2 versus ChAdOx1.

Supplemental material

Data and code availability.

All analytic code for the study is available in GitHub ( https://github.com/oxford-pharmacoepi/vaccineEffectOnPostCovidCardiacThromboembolicEvents ), including code lists for vaccines, COVID-19 tests and diagnoses, cardiac and thromboembolic events, NCO and health conditions to prioritise patients for vaccination in each country. We used R version 4.2.3 and statistical packages survival (3.5–3), Empirical Calibration (3.1.1), glmnet (4.1-7), and Hmisc (5.0–1).

Patient and public involvement

Owing to the nature of the study and the limitations regarding data privacy, the study design, analysis, interpretation of data and revision of the manuscript did not involve any patients or members of the public.

All aggregated results are available in a web application ( https://dpa-pde-oxford.shinyapps.io/PostCovidComplications/ ).

We included over 10.17 million vaccinated individuals (1 618 395 from CPRD Gold; 5 729 800 from CPRD Aurum; 2 744 821 from SIDIAP and 77 603 from CORIVA) and 10.39 million unvaccinated individuals (1 640 371; 5 860 564; 2 588 518 and 302 267, respectively). Online supplemental figures S2-5 illustrate study inclusion for each database.

Adequate covariate balance was achieved after PS weighting in most studies: CORIVA (all cohorts) and SIDIAP (cohorts 1 and 4) did not contribute to ChAdOx1 subanalyses owing to sample size and covariate imbalance. ASMD results are accessible in the web application.

NCO analyses suggested residual bias after PS weighting, with a majority of NCOs associated positively with vaccination. Therefore, calibrated estimates are reported in this manuscript. Uncalibrated effect estimates and NCO analyses are available in the web interface.

Population characteristics

Table 1 presents baseline characteristics for the weighted populations in CPRD Aurum, for illustrative purposes. Online supplemental tables S1-25 summarise baseline characteristics for weighted and unweighted populations for each database and comparison. Across databases and cohorts, populations followed similar patterns: cohort 1 represented an older subpopulation (around 80 years old) with a high proportion of women (57%). Median age was lowest in cohort 4 ranging between 30 and 40 years.

• View inline

Characteristics of weighted populations in CPRD Aurum database, stratified by staggered cohort and exposure status. Exposure is any COVID-19 vaccine

COVID-19 vaccination and post-COVID-19 complications

Table 2 shows the incidence of post-COVID-19 VTE, ATE and HF, the three most common post-COVID-19 conditions among the studied outcomes. Outcome counts are presented separately for 0–30, 31–90, 91–180 and 181–365 days after SARS-CoV-2 infection. Online supplemental tables S26-36 include all studied complications, also for the sensitivity and subanalyses. Similar pattern for incidences were observed across all databases: higher outcome rates in the older populations (cohort 1) and decreasing frequency with increasing time after infection in all cohorts.

Number of records (and risk per 10 000 individuals) for acute and post-acute COVID-19 cardiac and thromboembolic complications, across cohorts and databases for any COVID-19 vaccination

Forest plots for the effect of COVID-19 vaccines on post-COVID-19 cardiac and thromboembolic complications; meta-analysis across cohorts and databases. Dashed line represents a level of heterogeneity I 2 >0.4. ATE, arterial thrombosis/thromboembolism; CD+HS, cardiac diseases and haemorrhagic stroke; VTE, venous thromboembolism.

Results from calibrated estimates pooled in meta-analysis across cohorts and databases are shown in figure 2 .

Reduced risk associated with vaccination is observed for acute and post-acute VTE, DVT, and PE: acute meta-analytic sHR are 0.22 (95% CI, 0.17–0.29); 0.36 (0.28–0.45); and 0.19 (0.15–0.25), respectively. For VTE in the post-acute phase, sHR estimates are 0.43 (0.34–0.53), 0.53 (0.40–0.70) and 0.50 (0.36–0.70) for 31–90, 91–180, and 181–365 days post COVID-19, respectively. Reduced risk of VTE outcomes was observed in vaccinated across databases and cohorts, see online supplemental figures S14–22 .

Similarly, the risk of ATE, IS and MI in the acute phase after infection was reduced for the vaccinated group, sHR of 0.53 (0.44–0.63), 0.55 (0.43–0.70) and 0.49 (0.38–0.62), respectively. Reduced risk associated with vaccination persisted for post-acute ATE, with sHR of 0.74 (0.60–0.92), 0.72 (0.58–0.88) and 0.62 (0.48–0.80) for 31–90, 91–180 and 181–365 days post-COVID-19, respectively. Risk of post-acute MI remained lower for vaccinated in the 31–90 and 91–180 days after COVID-19, with sHR of 0.64 (0.46–0.87) and 0.64 (0.45–0.90), respectively. Vaccination effect on post-COVID-19 TIA was seen only in the 181–365 days, with sHR of 0.51 (0.31–0.82). Online supplemental figures S23-31 show database-specific and cohort-specific estimates for ATE-related complications.

Risk of post-COVID-19 cardiac complications was reduced in vaccinated individuals. Meta-analytic estimates in the acute phase showed sHR of 0.45 (0.38–0.53) for HF, 0.41 (0.26–0.66) for MP and 0.41 (0.27–0.63) for VACA. Reduced risk persisted for post-acute COVID-19 HF: sHR 0.61 (0.51–0.73) for 31–90 days, 0.61 (0.51–0.73) for 91–180 days and 0.52 (0.43–0.63) for 181–365 days. For post-acute MP, risk was only lowered in the first post-acute window (31–90 days), with sHR of 0.43 (0.21–0.85). Vaccination showed no association with post-COVID-19 HS. Database-specific and cohort-specific results for these cardiac diseases are shown in online supplemental figures S32-40 .

Stratified analyses by vaccine showed similar associations, except for ChAdOx1 which was not associated with reduced VTE and ATE risk in the last post-acute window. Sensitivity analyses were consistent with main results ( online supplemental figures S6-13 ).

Figure 3 shows the results of comparative effects of BNT162b2 versus ChAdOx1, based on UK data. Meta-analytic estimates favoured BNT162b2 (sHR of 0.66 (0.46–0.93)) for VTE in the 0–30 days after infection, but no differences were seen for post-acute VTE or for any of the other outcomes. Results from sensitivity analyses, database-specific and cohort-specific estimates were in line with the main findings ( online supplemental figures S41-51 ).

Forest plots for comparative vaccine effect (BNT162b2 vs ChAdOx1); meta-analysis across cohorts and databases. ATE, arterial thrombosis/thromboembolism; CD+HS, cardiac diseases and haemorrhagic stroke; VTE, venous thromboembolism.

Key findings

Our analyses showed a substantial reduction of risk (45–81%) for thromboembolic and cardiac events in the acute phase of COVID-19 associated with vaccination. This finding was consistent across four databases and three different European countries. Risks for post-acute COVID-19 VTE, ATE and HF were reduced to a lesser extent (24–58%), whereas a reduced risk for post-COVID-19 MP and VACA in vaccinated people was seen only in the acute phase.

Results in context

The relationship between SARS-CoV-2 infection, COVID-19 vaccines and thromboembolic and/or cardiac complications is tangled. Some large studies report an increased risk of VTE and ATE following both ChAdOx1 and BNT162b2 vaccination, 7 whereas other studies have not identified such a risk. 25 Elevated risk of VTE has also been reported among patients with COVID-19 and its occurrence can lead to poor prognosis and mortality. 26 27 Similarly, several observational studies have found an association between COVID-19 mRNA vaccination and a short-term increased risk of myocarditis, particularly among younger male individuals. 5 6 For instance, a self-controlled case series study conducted in England revealed about 30% increased risk of hospital admission due to myocarditis within 28 days following both ChAdOx1 and BNT162b2 vaccines. However, this same study also found a ninefold higher risk for myocarditis following a positive SARS-CoV-2 test, clearly offsetting the observed post-vaccine risk.

COVID-19 vaccines have demonstrated high efficacy and effectiveness in preventing infection and reducing the severity of acute-phase infection. However, with the emergence of newer variants of the virus, such as omicron, and the waning protective effect of the vaccine over time, there is a growing interest in understanding whether the vaccine can also reduce the risk of complications after breakthrough infections. Recent studies suggested that COVID-19 vaccination could potentially protect against acute post-COVID-19 cardiac and thromboembolic events. 11 12 A large prospective cohort study 11 reports risk of VTE after SARS-CoV-2 infection to be substantially reduced in fully vaccinated ambulatory patients. Likewise, Al-Aly et al 12 suggest a reduced risk for post-acute COVID-19 conditions in breakthrough infection versus SARS-CoV-2 infection without prior vaccination. However, the populations were limited to SARS-CoV-2 infected individuals and estimates did not include the effect of the vaccine to prevent COVID-19 in the first place. Other studies on post-acute COVID-19 conditions and symptoms have been conducted, 28 29 but there has been limited reporting on the condition-specific risks associated with COVID-19, even though the prognosis for different complications can vary significantly.

In line with previous studies, our findings suggest a potential benefit of vaccination in reducing the risk of post-COVID-19 thromboembolic and cardiac complications. We included broader populations, estimated the risk in both acute and post-acute infection phases and replicated these using four large independent observational databases. By pooling results across different settings, we provided the most up-to-date and robust evidence on this topic.

Strengths and limitations

The study has several strengths. Our multinational study covering different healthcare systems and settings showed consistent results across all databases, which highlights the robustness and replicability of our findings. All databases had complete recordings of vaccination status (date and vaccine) and are representative of the respective general population. Algorithms to identify study outcomes were used in previous published network studies, including regulatory-funded research. 3 4 8 18 Other strengths are the staggered cohort design which minimises confounding by indication and immortal time bias. PS overlap weighting and NCO empirical calibration have been shown to adequately minimise bias in vaccine effectiveness studies. 19 Furthermore, our estimates include the vaccine effectiveness against COVID-19, which is crucial in the pathway to experience post-COVID-19 complications.

Our study has some limitations. The use of real-world data comes with inherent limitations including data quality concerns and risk of confounding. To deal with these limitations, we employed state-of-the-art methods, including large-scale propensity score weighting and calibration of effect estimates using NCO. 19 24 A recent study 30 has demonstrated that methodologically sound observational studies based on routinely collected data can produce results similar to those of clinical trials. We acknowledge that results from NCO were positively associated with vaccination, and estimates might still be influenced by residual bias despite using calibration. Another limitation is potential under-reporting of post-COVID-19 complications: some asymptomatic and mild COVID-19 infections might have not been recorded. Additionally, post-COVID-19 outcomes of interest might be under-recorded in primary care databases (CPRD Aurum and Gold) without hospital linkage, which represent a large proportion of the data in the study. However, results in SIDIAP and CORIVA, which include secondary care data, were similar. Also, our study included a small number of young men and male teenagers, who were the main population concerned with increased risks of myocarditis/pericarditis following vaccination.

Conclusions

Vaccination against SARS-CoV-2 substantially reduced the risk of acute post-COVID-19 thromboembolic and cardiac complications, probably through a reduction in the risk of SARS-CoV-2 infection and the severity of COVID-19 disease due to vaccine-induced immunity. Reduced risk in vaccinated people lasted for up to 1 year for post-COVID-19 VTE, ATE and HF, but not clearly for other complications. Findings from this study highlight yet another benefit of COVID-19 vaccination. However, further research is needed on the possible waning of the risk reduction over time and on the impact of booster vaccination.

Ethics statements

Patient consent for publication.

Not applicable.

Ethics approval

The study was approved by the CPRD’s Research Data Governance Process, Protocol No 21_000557 and the Clinical Research Ethics committee of Fundació Institut Universitari per a la recerca a l’Atenció Primària de Salut Jordi Gol i Gurina (IDIAPJGol) (approval number 4R22/133) and the Research Ethics Committee of the University of Tartu (approval No. 330/T-10).

Acknowledgments

This study is based in part on data from the Clinical Practice Research Datalink (CPRD) obtained under licence from the UK Medicines and Healthcare products Regulatory Agency. We thank the patients who provided these data, and the NHS who collected the data as part of their care and support. All interpretations, conclusions and views expressed in this publication are those of the authors alone and not necessarily those of CPRD. We would also like to thank the healthcare professionals in the Catalan healthcare system involved in the management of COVID-19 during these challenging times, from primary care to intensive care units; the Institut de Català de la Salut and the Program d’Analítica de Dades per a la Recerca i la Innovació en Salut for providing access to the different data sources accessible through The System for the Development of Research in Primary Care (SIDIAP).

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Supplementary materials

Supplementary data.

This web only file has been produced by the BMJ Publishing Group from an electronic file supplied by the author(s) and has not been edited for content.

• Data supplement 1

AMJ and MC are joint senior authors.

Contributors DPA and AMJ led the conceptualisation of the study with contributions from MC and NM-B. AMJ, TD-S, ER, AU and NTHT adapted the study design with respect to the local vaccine rollouts. AD and WYM mapped and curated CPRD data. MC and NM-B developed code with methodological contributions advice from MTS-S and CP. DPA, MC, NTHT, TD-S, HMEN, XL, CR and AMJ clinically interpreted the results. NM-B, XL, AMJ and DPA wrote the first draft of the manuscript, and all authors read, revised and approved the final version. DPA and AMJ obtained the funding for this research. DPA is responsible for the overall content as guarantor: he accepts full responsibility for the work and the conduct of the study, had access to the data, and controlled the decision to publish.

Funding The research was supported by the National Institute for Health and Care Research (NIHR) Oxford Biomedical Research Centre (BRC). DPA is funded through a NIHR Senior Research Fellowship (Grant number SRF-2018–11-ST2-004). Funding to perform the study in the SIDIAP database was provided by the Real World Epidemiology (RWEpi) research group at IDIAPJGol. Costs of databases mapping to OMOP CDM were covered by the European Health Data and Evidence Network (EHDEN).

Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting or dissemination plans of this research.

Provenance and peer review Not commissioned; externally peer reviewed.

Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.

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Posts Make Ominous, Unfounded Claims About April 8 Eclipse Preparations

By Alan Jaffe and Hadleigh Zinsner

Posted on March 22, 2024

Para leer en español, vea esta traducción de Google Translate.

Local governments are preparing residents for an influx of visitors during the April 8 solar eclipse that will be most visible along a narrow path through the U.S., with one Oklahoma county inviting the National Guard for support. But social media posts baselessly claim the preparations suggest “something catastrophic” will occur during the eclipse.

A total solar eclipse — in which the moon briefly blocks the face of the sun — will be visible on a narrow path from western Mexico, through the United States, and into Maritime Canada on April 8. At locations along the “path of totality” where the astronomical alignment can be best viewed, the full eclipse will last four and a half minutes. The last time the U.S. experienced a total eclipse was in August 2017, and the next opportunity to see one in the U.S. will be in August 2044.

National agencies and local governments have been preparing for the impact the event will have on towns along the path of the total eclipse due to the number of visitors expected at those locations.

In advance of the partial eclipse in 2023 and the total eclipse in 2024, the U.S. Department of Transportation published a fact sheet that explained, “Because a solar eclipse is a relatively rare type of planned special event, it can generate large volumes of traffic for which State and local departments of transportation (DOTs) will need to prepare.” That fact sheet also noted that the total eclipse in 2017 “created delays and queuing on rural interstates and highways across the Nation.”

The health department of Oswego County, New York , like many counties that will have a view of the total eclipse, has suggested that residents fill up vehicle gasoline tanks and buy groceries before visitors arrive in the area. Lorain County, Ohio, has advised that cell phone signals may be lost “due to system overload” caused by the influx of visitors. Many school districts will close or have early dismissals to allow students to experience the eclipse.

But some social media posts are making unfounded claims that the government preparations for the eclipse are signs of something ominous.

Counties Anticipate Crowds, Call in Support

The text on a March 19 Instagram post reads, “1 month Before the ECLIPSE They are Declaring State of Disaster!” An unidentified woman in the video in the post says, in part, “What in the world is really going on? A month before the eclipse, Travis County [Texas] declares a state of emergency, and also asks for help because they believe their hospitals are going to be full. There’s going to be a lot of chaos going around. Schools are going to be closed. … No signal. Something just doesn’t add up. We’ve had eclipses before and we’ve never seen this type of stuff.”

Another Instagram post about preparations in Travis County, Texas, misleadingly claims , “They know something catastrophic will happen.”

It’s true that Travis County, Texas, issued a disaster declaration on March 8. The city of Lago Vista explained why on its website on March 11: “Travis County Judge Andy Brown declared a local state of disaster in anticipation of extremely large crowds, increased traffic and strains on first responders, hospitals and roads since we are in the direct path of totality for the eclipse. This disaster declaration will allow first responders and public safety officials to better manage traffic and crowds as we are expected to have our population double in size for this once in a lifetime phenomenon.”

A viral TikTok post shared on Facebook questions why McCurtain County, Oklahoma, is calling up the National Guard during the eclipse. “This is getting wild. The National Guard is going to be here now for the solar eclipse. … But things get much weirder.” The video’s narrator then says “an elite chemical, biological, radiological and nuclear unit” also will be housed nearby during the eclipse. The narrator adds, “People are going on Twitter making statements like this, ‘Something strange is definitely happening.'”

Oklahoma National Guard troops will indeed be on hand during the event, and a statement from the Guard explained their role.

“McCurtain County Emergency Management requested our support because they expect up to 100,000 additional people visiting their communities to watch the eclipse,” Lt. Col. Jabonn Flurry, commander of the 63rd Civil Support Team, said in a March 18 press release from the Oklahoma National Guard. “This influx of visitors has the potential to overtax local resources and thanks to the training and experience our Guardsmen have working alongside local agencies all across Oklahoma, the CST is uniquely qualified to support our fellow Oklahomans.” 

The press release also said, “In the event of a HAZMAT emergency like an industrial fire that requires specialized training, the 63rd CST’s resources will respond, allowing local emergency responders to continue their assistance to citizens and the expected increase of visitors.”

The release didn’t mention the post’s claim about an “elite chemical, biological, radiological and nuclear unit,” but it noted: “Members of the 63rd CST receive more than 650 hours of HAZMAT and high-tech training from agencies such as the Federal Emergency Management Agency, the Department of Energy, the Department of Justice, and the Environmental Protection Agency.” 

This is not the first time local governments have geared up for the impact of an eclipse, contrary to what some social media posts claim. The Oregon Office of Emergency Management prepared for a year ahead of the 2017 eclipse. The National Park Service suggested stocking up with food, water and gas in preparation for viewing the 2017 eclipse in Grand Teton National Park. The state of Wyoming also experienced unanticipated, record-breaking traffic jams after the eclipse that year.

NASA recommends that everyone viewing the eclipse follow health and safety measures, including the use of specialized eye protection or indirect viewing equipment.

Editor’s note:  FactCheck.org  is one of several organizations  working with Facebook  to debunk misinformation shared on social media. Our previous stories can be found  here . Facebook has  no control  over our editorial content.

City of Lago Vista, Texas. “Disaster Declaration issued ahead of the 4/8/24 Solar Eclipse.” 11 Mar 2024.

Lorain County, Ohio, Commissioners. “April 8th, 2024 Total Solar Eclipse.” Accessed 21 Mar 2024.

McCullough, Erin. “Rutherford County Schools closing for solar eclipse April 8.” WKRN. 21 Mar 2024.

NASA. “2024 Total Solar Eclipse.” Accessed 20 Mar 2024.

NASA. “Eclipse Safety.” Accessed 21 Mar 2024.

National Park Service. Grand Teton National Park. “2017 Total Solar Eclipse.” 21 Aug 2017.

Oklahoma National Guard. Press release. “Oklahoma National Guard to assist McCurtain County amid influx of eclipse tourism.” 18 Mar 2024.

Oregon Department of Emergency Management. “Hazards and Preparedness: 2017 Total Solar Eclipse.” Accessed 22 Mar 2024.

Oswego County Health Department. “Be Ready For Total Solar Eclipse On April 8.” 21 Feb 2024.

Peek, Katie. “Here Are the Best Places to View the 2024 Total Solar Eclipse.” Scientific American. 2 Feb 2024.

Rainey, Libby. “Wyoming solar eclipse traffic jam was one for the record books.” Denver Post. Updated 23 Aug 2017.

Somers, Jennifer. “These St. Louis-area schools will be closed for the April 8 solar eclipse.” KSDK-TV. Updated 21 Mar 2024.

Travis County, Texas. “Travis County Declaration of Local Disaster Due April 8, 2024 Solar Eclipse.” 8 Mar 2024.

U.S. Department of Transportation. Fact sheet. “Preparing for a Solar Eclipse.” Accessed 21 Mar 2024.

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Features, evaluation, and treatment of coronavirus (covid-19).

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• Continuing Education Activity

Coronavirus disease 2019 (COVID-19) is a highly contagious infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). COVID-19 has had a catastrophic effect on the world, resulting in more than 6 million deaths worldwide. It has emerged as the most consequential global health crisis since the era of the influenza pandemic of 1918. As the virus mutates, treatment guidelines are altered to reflect the most efficacious therapies. This activity is a comprehensive review of the disease presentation, complications, and current guideline-recommended treatment options for managing this disease.

• Screen individuals based on exposure and symptom criteria to identify potential COVID-19 cases.
• Identify the clinical features and radiological findings expected in patients with COVID-19.
• Apply the recommended treatment options for patients with COVID-19.
• Create strategies with the interprofessional team for improving care coordination to care for patients with COVID-19 to help improve clinical outcomes.
• Introduction

Coronavirus disease 2019 (COVID-19) is a highly contagious viral illness caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). COVID-19 has had a catastrophic effect on the world, resulting in more than 6 million deaths worldwide. After the first cases of this predominantly respiratory viral illness were reported in Wuhan, Hubei Province, China, in late December 2019, SARS-CoV-2 rapidly disseminated worldwide. This compelled the World Health Organization (WHO) to declare it a global pandemic on March 11, 2020. [1]

Even though substantial progress in clinical research has led to a better understanding of SARS-CoV-2, many countries continue to have outbreaks of this viral illness. These outbreaks are primarily attributed to the emergence of mutant variants of the virus. Like other RNA viruses, SARS-CoV-2 adapts with genetic evolution and developing mutations. This results in mutant variants that may have different characteristics than their ancestral strains. Several variants of SARS-CoV-2 have been described during the course of this pandemic, among which only a few are considered variants of concern (VOCs). Based on the epidemiological update by the WHO, 5 SARS-CoV-2 VOCs have been identified since the beginning of the pandemic:

• Alpha (B.1.1.7): First variant of concern, which was described in the United Kingdom (UK) in late December 2020 [2]
• Beta (B.1.351) : First reported in South Africa in December 2020 [2]
• Gamma (P.1) : First reported in Brazil in early January 2021 [2]
• Delta (B.1.617.2):  First reported in India in December 2020 [2]
• Omicron   (B.1.1.529): First reported in South Africa in November 2021 [3]

Despite the unprecedented speed of vaccine development against the prevention of COVID-19 and robust global mass vaccination efforts, the emergence of new SARS-CoV-2 variants threatens to overturn the progress made in limiting the spread of this disease. This review aims to comprehensively describe the etiology, epidemiology, pathophysiology, and clinical features of COVID-19. This review also provides an overview of the different variants of SARS-CoV-2 and the guideline-recommended treatment (as of January 2023) for managing this disease. 

Coronaviruses (CoVs) are positive-sense single-stranded RNA (+ssRNA) viruses with a crown-like appearance under an electron microscope ( coronam  is the Latin term for crown) due to the presence of spike glycoproteins on the envelope. [1] The subfamily  Orthocoronavirinae  of the  Coronaviridae  family (order  Nidovirales ) classifies into 4 genera of CoVs: 

• Alphacoronavirus (alphaCoV)
• Betacoronavirus (betaCoV)
• Deltacoronavirus (deltaCoV)
• Gammacoronavirus (gammaCoV)

BetaCoV genus is further divided into 5 sub-genera or lineages. [4]  Genomic characterization has shown that bats and rodents are the probable gene sources of alphaCoVs and betaCoVs. Avian species seem to be the source of deltaCoVs and gammaCoVs. CoVs have become significant pathogens of emerging respiratory disease outbreaks. Members of this large family of viruses can cause respiratory, enteric, hepatic, and neurological diseases in different animal species, including camels, cattle, cats, and bats.

These viruses can cross species barriers and infect humans as well. Seven human CoVs (HCoVs) capable of infecting humans have been identified. Some HCoVs were identified in the mid-1960s, while others were only detected in the new millennium. In general, estimates suggest that 2% of the population are healthy carriers of CoVs and that these viruses are responsible for about 5% to 10% of acute respiratory infections. [5]  

• Common human CoVs : HCoV-OC43 and HCoV-HKU1 (betaCoVs of the A lineage), HCoV-229E, and HCoV-NL63 (alphaCoVs). These viruses can cause common colds and self-limiting upper respiratory tract infections in immunocompetent individuals. However, in immunocompromised and older patients, lower respiratory tract infections can occur due to these viruses.
• Other human CoVs : SARS-CoV and MERS-CoV (betaCoVs of the B and C lineage, respectively). These viruses are considered more virulent and capable of causing epidemics with respiratory and extra-respiratory manifestations of variable clinical severity. [1]  

SARS-CoV-2 is a novel betaCoV belonging to the same subgenus as the severe acute respiratory syndrome coronavirus (SARS-CoV) and the Middle East Respiratory Syndrome Coronavirus (MERS-CoV), which have been previously implicated in SARS-CoV and MERS-CoV epidemics with mortality rates up to 10% and 35%, respectively. [6]  It has a round or elliptic and often pleomorphic form and a diameter of approximately 60 to 140 nm. Like other CoVs, it is sensitive to ultraviolet rays and heat. [6]  

The inactivation temperature of SARS-CoV-2 is being researched. A stainless steel surface held at an air temperature of 54.5°C (130 °F) results in the inactivation of 90% of SARS-CoV-2 in approximately 36 minutes. [7]  It resists lower temperatures, even those below 0°C. However, lipid solvents can effectively inactivate these viruses, including ether (75%), ethanol, chlorine-containing disinfectant, peroxyacetic acid, and chloroform (except for chlorhexidine).

Although the origin of SARS-CoV-2 is currently unknown, it is widely postulated to have a zoonotic transmission. [1]  Genomic analyses suggest that SARS-CoV-2 probably evolved from a strain found in bats. The genomic comparison between the human SARS-CoV-2 sequence and known animal coronaviruses revealed high homology (96%) between the SARS-CoV-2 and the betaCoV RaTG13 of bats ( Rhinolophus affinis ). [8]  Similar to SARS and MERS, it has been hypothesized that SARS-CoV-2 advanced from bats to intermediate hosts, such as pangolins and minks, and then to humans. [9] [10]

SARS-CoV-2 Variants

A globally dominant D614G variant was eventually identified and associated with increased transmissibility but without the ability to cause severe illness. [11] Another variant was attributed to transmission from infected farmed mink in Denmark but was not associated with increased transmissibility. [10]  Since then, multiple variants of SARS-CoV-2 have been described, of which a few are considered variants of concern (VOCs) due to their potential to cause enhanced transmissibility or virulence. The United States Centers for Disease Control and Prevention (CDC) and the WHO have independently established a classification system for distinguishing the emerging variants of SARS-CoV-2 into variants of concern(VOCs) and variants of interest(VOIs).

SARS-CoV-2 Variants of Concern (VOCs)

• Alpha (B.1.1.7 lineage)
• In late December 2020, the Alpha variant,   or GRY  (formerly GR/501Y.V1), was reported in the UK based on whole-genome sequencing of samples from patients who tested positive for SARS-CoV-2. [12] [13]
• The variant   was also identified using a commercial assay characterized by the absence of the S gene (S-gene target failure, SGTF) in PCR samples. The B.1.1.7 variant includes 17 mutations in the viral genome. Of these, 8 mutations (Δ69-70 deletion, Δ144 deletion, N501Y, A570D, P681H, T716I, S982A, D1118H) are in the spike (S) protein. N501Y shows an increased affinity of the spike protein to ACE 2 receptors, enhancing the viral attachment and subsequent entry into host cells. [14] [15] [16]
• This alpha variant was reportedly 43% to 82% more transmissible, surpassing preexisting variants of SARS-CoV-2 to emerge as the dominant SARS-CoV-2 variant in the UK. [15]  
• An initial matched case-control study reported no significant difference in the risk of hospitalization or associated mortality with the B.1.1.7 lineage variant compared to other existing variants. However, subsequent studies have reported that people infected with B.1.1.7 lineage variant had increased disease severity compared to those infected with other circulating variants. [17] [13]  
• A large matched cohort study in the UK reported that the mortality hazard ratio of patients infected with the B.1.1.7 lineage variant was 1.64 (95% confidence interval 1.32 to 2.04, P<0.0001) compared to patients with previously circulating strains. [18]
• Another study reported that the B 1.1.7 variant was associated with increased mortality compared to other SARS-CoV-2 variants (HR= 1.61, 95% CI 1.42-1.82). [19]  The risk of death was reportedly greater (adjusted hazard ratio 1.67, 95% CI 1.34-2.09) among individuals with confirmed B.1.1.7 infection compared to individuals with non-B.1.1.7 SARS-CoV-2. [20]
• Beta (B.1.351 lineage)
• The Beta variant, or GH501Y.V2 with multiple spike mutations, resulted in the second wave of COVID-19 infections and was first detected in South Africa in October 2020. [21]
• The B.1.351 variant includes 9 mutations (L18F, D80A, D215G, R246I, K417N, E484K, N501Y, D614G, and A701V) in the spike protein, of which 3 mutations (K417N, E484K, and N501Y) are located in the receptor binding domain (RBD) and increase its binding affinity for the ACE receptors. [22] [14] [23]  
• SARS-CoV-2 501Y.V2 (B.1.351 lineage) was reported in the US at the end of January 2021.
• This variant had an increased risk of transmission and reduced neutralization by monoclonal antibody therapy, convalescent sera, and post-vaccination sera. [24]
• Gamma (P.1 lineage)
• The Gamma variant, or  GR/501Y.V3 , was identified in December 2020 in Brazil and was first detected in the US in January 2021. [25]  
• This B.1.1.28 variant harbors ten mutations in the spike protein (L18F, T20N, P26S, D138Y, R190S, H655Y, T1027I V1176, K417T, E484K, and N501Y). Three mutations (L18F, K417N, E484K) are located in the RBD, similar to the B.1.351 variant. [25]
• The Delta variant was initially identified in December 2020 in India and was responsible for the deadly second wave of COVID-19 infections in April 2021 in India. In the United States, this variant was first detected in March 2021. [2]
• The B.1.617.2 variant harbors ten mutations ( T19R, (G142D*), 156del, 157del, R158G, L452R, T478K, D614G, P681R, D950N) in the spike protein.
• The Omicron variant was first identified in South Africa on 23 November 2021 after an uptick in the number of cases of COVID-19. [26]  
• Omicron was quickly recognized as a VOC due to more than 30 changes to the spike protein of the virus and the sharp rise in the number of cases observed in South Africa. [27]  The reported mutations include T91 in the envelope, P13L, E31del, R32del, S33del, R203K, G204R in the nucleocapsid protein, D3G, Q19E, A63T in the matrix, N211del/L212I, Y145del, Y144del, Y143del, G142D, T95I, V70del, H69del, A67V in the N-terminal domain of the spike, Y505H, N501Y, Q498R, G496S, Q493R, E484A, T478K, S477N, G446S, N440K, K417N, S375F, S373P, S371L, G339D in the receptor-binding domain of the spike, D796Y in the fusion peptide of the spike, L981F, N969K, Q954H in the heptad repeat 1 of the spike as well as multiple other mutations in the non-structural proteins and spike protein. [28]
• Many subvariants of Omicron, such as BA.1, BA.2, BA.3, BA.4, and BA.5, have been identified. [3]

Transmission of SARS-CoV-2

• The primary mode of transmission of SARS-CoV-2 is via exposure to respiratory droplets carrying the infectious virus from close contact or direct transmission from presymptomatic, asymptomatic, or symptomatic individuals harboring the virus. [1]
• Airborne transmission with aerosol-generating procedures has also been implicated in the spread of COVID-19. Data implicating airborne transmission of SARS-CoV-2 in the absence of aerosol-generating procedures is present; however, this mode of transmission has not been universally acknowledged.
• Fomite transmission from contamination of inanimate surfaces with SARS-CoV-2 has been well characterized based on many studies reporting the viability of SARS-CoV-2 on various porous and nonporous surfaces. Under experimental conditions, SARS-CoV-2 was stable on stainless steel and plastic surfaces compared to copper and cardboard surfaces, with the viable virus being detected up to 72 hours after inoculating the surfaces with the virus. [29]  The viable virus was isolated for up to 28 days at 20°C from nonporous surfaces such as glass and stainless steel. Conversely, recovery of SARS-CoV-2 on porous materials was reduced compared with nonporous surfaces. [30]  In hospital settings, the SARS-CoV-2 has been detected on floors, computer mice, trash cans, sickbed handrails, and in the air (up to 4 meters from patients). [31]  The Centers for Disease Control and Prevention (CDC) has stated that individuals can be infected with SARS-CoV-2 via contact with surfaces contaminated by the virus, but the risk is low and is not the main route of transmission of this virus.
• Epidemiologic data from several case studies have reported that patients with SARS-CoV-2 infection have the live virus in feces implying possible fecal-oral transmission. [32]
• A meta-analysis that included 936 neonates from mothers with COVID-19 showed vertical transmission is possible but occurs in a minority of cases. [33]
• Epidemiology

COVID-19 was the third leading cause of death in the United States (USA) in 2020 after heart disease and cancer, with approximately 375,000 deaths. [34]  

Individuals of all ages are at risk of contracting this infection. However, patients aged ≥60 and patients with underlying medical comorbidities (obesity, cardiovascular disease, chronic kidney disease, diabetes, chronic lung disease, smoking, cancer, solid organ or hematopoietic stem cell transplant patients) have an increased risk of developing severe COVID-19 infection.

According to the CDC, age remains the strongest predictor of poor outcomes and severe illness in patients with COVID-19. Data from the National Vital Statistics System (NVSS) at CDC states that patients with COVID-19 aged 50 to 64 years have a 25 times higher risk of death when compared to adults infected with this illness and aged less than 30 years. In patients 65 to 74 years old, this risk increases to 60 times. In patients older than 85, the risk of death increases to 340 times. According to the CDC, these data include all deaths in the United States throughout the pandemic, from February 2020 to July 1, 2022, including deaths among unvaccinated individuals.

The percentage of COVID-19 patients requiring hospitalization was 6 times higher in those with preexisting medical conditions than those without medical conditions (45.4% vs. 7.6%) based on an analysis by Stokes et al. of confirmed cases reported to the CDC from January 22 to May 30, 2020. [35]  The study also reported that the percentage of patients who succumbed to this illness was 12 times higher in those with preexisting medical conditions than those without (19.5% vs 1.6%). [35]  

Data regarding the gender-based differences in COVID-19 suggests that male patients have a higher risk of severe illness and increased mortality due to COVID-19 compared to female patients. [36] [37]  Results from a retrospective cohort study from March 1 to November 21, 2020, evaluating the mortality rate in 209 United States of America (USA) acute care hospitals that included 42604 patients with confirmed SARS-CoV-2 infection, reported a higher mortality rate in male patients (12.5%) compared to female patients (9.6%). [38]

Racial and ethnic minority groups have been reported to have a higher percentage of COVID-19-related hospitalizations than White patients based on a recent CDC analysis of hospitalizations from an extensive administrative database that included approximately 300,000 COVID-19 patients hospitalized from March 2020 to December 2020. This high percentage of COVID-19-related hospitalizations among racial and ethnic groups was driven by a higher risk of exposure to SARS-CoV-2 and an increased risk of developing severe COVID-19 disease. [39]   A meta-analysis of 50 studies from USA and UK researchers noted that people of Black, Hispanic, and Asian ethnic minority groups are at increased risk of contracting and dying from COVID-19 infection. [40]  

COVID-19-related death rates were the highest among Hispanic persons. [34]  Another analysis by the CDC evaluating the risk of COVID-19 among sexual minority adults reported that underlying medical comorbidities which increase the risk of developing severe COVID-19 were more prevalent in sexual minority individuals than heterosexual individuals within the general population and within specific racial/ethnic groups. [41]

• Pathophysiology

Structurally and phylogenetically, SARS-CoV-2 is similar to SARS-CoV and MERS-CoV and is composed of 4 main structural proteins: spike (S), envelope (E) glycoprotein, nucleocapsid (N), and membrane (M) protein. It also contains 16 nonstructural proteins and 5-8 accessory proteins. [42]  

The surface spike (S) glycoprotein, which resembles a crown, is located on the outer surface of the virion. It undergoes cleavage into an amino (N)-terminal S1 subunit, which facilitates the incorporation of the virus into the host cell. The carboxyl (C)-terminal S2 subunit contains a fusion peptide, a transmembrane domain, and a cytoplasmic domain responsible for virus-cell membrane fusion. [43] [44]  The S1 subunit is further divided into a receptor-binding domain (RBD) and an N-terminal domain (NTD), which facilitates viral entry into the host cell and serves as a potential target for neutralization in response to antisera or vaccines . [45]  

The RBD is a fundamental peptide in the pathogenesis of infection as it represents a binding site for the human angiotensin-converting enzyme 2 (ACE2) receptors. Inhibition of the renin-angiotensin-aldosterone system (RAAS) does not increase the risk of hospitalization for COVID-19 and severe disease. [46]

SARS-CoV-2 gains entry into the host cells by binding the SARS-CoV-2 spike or S protein (S1) to the ACE2 receptors in the respiratory epithelium. ACE2 receptors are also expressed by other organs such as the upper esophagus, enterocytes from the ileum, myocardial cells, proximal tubular cells of the kidney, and urothelial cells of the bladder. [47]  The viral attachment process is followed by priming the spike protein S2 subunit by the host transmembrane serine protease 2 (TMPRSS2) that facilitates cell entry and subsequent viral replication. [48]

In the early phase of the infection, viral replication results in direct virus-mediated tissue damage. In the late phase, the infected host cells trigger an immune response by recruiting T lymphocytes, monocytes, and neutrophils. Cytokines such as tumor necrosis factor-α (TNF α), granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-1 (IL-1), interleukin-6 (IL-6), ), IL-1β, IL-8, IL-12 and interferon (IFN)-γ are released. In severe COVID-19 illness, a 'cytokine storm' is seen. This is due to the over-activation of the immune system and high levels of cytokines in circulation. This results in a local and systemic inflammatory response. [49] [50]  

Effect of SARS-CoV-2 on the Respiratory System

Increased vascular permeability and subsequent development of pulmonary edema in patients with severe COVID-19 are explained by multiple mechanisms. [51] [52] [53]  These mechanisms include:

• Endotheliitis as a result of direct viral injury and perivascular inflammation leading to microvascular and microthrombi deposition
• Dysregulation of RAAS due to increased binding of the virus to the ACE2 receptors
• Activation of the kallikrein-bradykinin pathway, the activation of which enhances vascular permeability
• Enhanced epithelial cell contraction causes swelling of cells and disturbance of intercellular junctions
• The binding of SARS-CoV-2 to the Toll-Like Receptor (TLR) induces the release of pro-IL-1β, which mediates lung inflammation until fibrosis . [54]

Effect of SARS-CoV-2 on Extrapulmonary Organ Systems

Although the respiratory system is the principal target for SARS-CoV-2, other major organ systems such as the gastrointestinal tract (GI), hepatobiliary, cardiovascular, renal, and central nervous systems may also be affected. SARS-CoV-2–induced organ dysfunction is likely due to a combination of mechanisms, such as direct viral toxicity, ischemic injury caused by vasculitis, thrombosis, immune dysregulation, and renin-angiotensin-aldosterone system (RAAS) dysregulation. [55]

Cardiac involvement in COVID-19 is common and likely multifactorial. ACE2 receptors exhibited by myocardial cells may cause direct cytotoxicity to the myocardium leading to myocarditis. Proinflammatory cytokines such as IL-6 can also lead to vascular inflammation, myocarditis, and cardiac arrhythmias. [56]

Acute coronary syndrome (ACS) is a well-recognized cardiac manifestation of COVID-19. It is likely due to multiple factors, including proinflammatory cytokines, worsening of preexisting severe coronary artery disease, coronary plaque destabilization, microthrombogenesis, and reduced coronary blood flow. [57]  

SARS-CoV-2 has a significant effect on the hematological and hemostatic systems as well. The mechanism of leukopenia, one of the most common laboratory abnormalities encountered in COVID-19, is unknown. Several hypotheses have been postulated that include ACE 2 mediated lymphocyte destruction by direct invasion by the virus, lymphocyte apoptosis due to proinflammatory cytokines, and possible invasion of the virus in the lymphatic organs. [58]  

Thrombocytopenia is common in COVID-19 and is likely due to multiple factors, including virus-mediated suppression of platelets, autoantibodies formation, and coagulation cascade activation, resulting in platelet consumption. [59]  

Thrombocytopenia and neutrophilia are considered a hallmark of severe illness. [55] Although it is well known that COVID-19 is associated with a state of hypercoagulability, the exact mechanisms that lead to the activation of the coagulation system are unknown and likely attributed to the cytokine-induced inflammatory response. The pathogenesis of this associated hypercoagulability is multifactorial. The hypercoagulability is probably induced by direct viral-mediated damage or cytokine-induced injury of the vascular endothelium leading to the activation of platelets, monocytes, and macrophages, with increased expression of von Willebrand factor and Factor VIII that results in the generation of thrombin and formation of a fibrin clot. [59] [60]  

Other mechanisms that have been proposed include possible mononuclear phagocyte-induced prothrombotic sequelae, derangements in the renin-angiotensin system (RAS) pathways, and complement-mediated microangiopathy. [59]

• History and Physical

Clinical Manifestations of COVID-19

• The median incubation period for SARS-CoV-2 is estimated to be 5.1 days, and most patients will develop symptoms within 11.5 days of infection. [61]
• The clinical spectrum of COVID-19 varies from asymptomatic or paucisymptomatic forms to clinical illness characterized by acute respiratory failure requiring mechanical ventilation, septic shock, and multiple organ failure. 
• It is estimated that 17.9% to 33.3% of infected patients will remain asymptomatic. [62] [63]
• Most symptomatic patients present with fever, cough, and shortness of breath. Less common symptoms include sore throat, anosmia, dysgeusia, anorexia, nausea, malaise, myalgias, and diarrhea. Stokes et al. reported that among 373,883 confirmed symptomatic COVID-19 cases in the USA, 70% experienced fever, cough, and shortness of breath, 36% reported myalgia, and 34% reported headache. [35]
• A large meta-analysis evaluating clinicopathological characteristics of 8697 patients with COVID-19 in China reported laboratory abnormalities that included lymphopenia (47.6%), elevated C-reactive protein levels (65.9%), elevated cardiac enzymes (49.4%), and abnormal liver function tests (26.4%). Other laboratory abnormalities included leukopenia (23.5%), elevated D-dimer (20.4%), elevated erythrocyte sedimentation rate (20.4%), leukocytosis (9.9%), elevated procalcitonin (16.7%), and abnormal renal function (10.9%). [64]
• A meta-analysis of 212 published studies with 281,461 individuals from 11 countries/regions reported that severe disease course was noted in about 23% of the patients, with a mortality rate of about 6% in patients infected with COVID-19. [65]
• An elevated neutrophil-to-lymphocyte ratio (NLR), an elevated derived NLR ratio (d-NLR), and an elevated platelet-to-lymphocyte ratio indicate a cytokine-induced inflammatory storm. [66]

Based on the severity of the presenting illness, which includes clinical symptoms, laboratory and radiographic abnormalities, hemodynamics, and organ function, the National Institutes of Health (NIH) issued guidelines that classify COVID-19 into 5 distinct types.[ NIH COVID-19 Treatment Guidelines ]

• Asymptomatic or Presymptomatic Infection : Individuals with positive SARS-CoV-2 test without any clinical symptoms consistent with COVID-19.
• Mild illness : Individuals who have symptoms of COVID-19, such as fever, cough, sore throat, malaise, headache, muscle pain, nausea, vomiting, diarrhea, anosmia, or dysgeusia but without shortness of breath or abnormal chest imaging.
• Moderate illness : Individuals with clinical symptoms or radiologic evidence of lower respiratory tract disease and oxygen saturation (SpO 2 ) ≥94% on room air.
• Severe illness : Individuals who have SpO 2 less than 94% on room air, a ratio of partial pressure of arterial oxygen to fraction of inspired oxygen (PaO 2 /FiO 2 ) of less than 300, marked tachypnea with a respiratory frequency of greater than 30 breaths/min, or lung infiltrates that are greater than 50% of total lung volume.
• Critical illness : Individuals with acute respiratory failure, septic shock, or multiple organ dysfunction. Patients with severe COVID-19 illness may become critically ill with the development of acute respiratory distress syndrome (ARDS). This tends to occur approximately one week after the onset of symptoms.

ARDS is characterized by a severe new-onset respiratory failure or worsening of an already identified respiratory picture. The diagnosis requires bilateral opacities (lung infiltrates >50%), not fully explained by effusions or atelectasis. The Berlin definition classifies ARDS into 3 types based on the degree of hypoxia, with the reference parameter being PaO 2 /FiO 2 or P/F ratio: [67]

• Mild ARDS : 200 mm Hg <PaO 2 /FiO 2 ≤300 mm Hg in patients not receiving mechanical ventilation or in those managed through noninvasive ventilation (NIV) by using positive end-expiratory pressure (PEEP) or a continuous positive airway pressure (CPAP) ≥5 cm H2O.
• Moderate ARDS : 100 mm Hg <PaO 2 /FiO 2 ≤200 mm Hg
• Severe ARDS : PaO 2 /FiO 2 ≤100 mm Hg

When PaO 2 is unavailable, a ratio of SpO 2 /FiO 2 ≤315 suggests ARDS. A multicenter prospective observational study that analyzed 28-day mortality in mechanically ventilated patients with ARDS concluded that COVID-19 patients with ARDS had features similar to other ARDS cohorts, and the risk of 28-day mortality increased with ARDS severity. [68]

Extrapulmonary Manifestations 

• Acute kidney injury (AKI) is the most frequently encountered extrapulmonary manifestation of COVID-19 and is associated with an increased mortality risk. [69] A large multicenter cohort study of hospitalized patients with COVID-19 that involved 5,449 patients admitted with COVID-19 reported that 1993 (36.6%) patients developed AKI during their hospitalization, of which 14.3% of patients required renal replacement therapy (RRT). [70]  
• Myocardial injury manifesting as myocardial ischemia/infarction (MI) and myocarditis are well-recognized cardiac manifestations in patients with COVID-19. Single-center retrospective study analysis of 187 patients with confirmed COVID-19 reported that 27.8% of patients exhibited myocardial injury indicated by elevated troponin levels. The study also noted that patients with elevated troponin levels had more frequent malignant arrhythmias and a higher mechanical ventilation frequency than patients with normal troponin levels. [71]  A meta-analysis of 198 published studies involving 159698 COVID-19 patients reported that acute myocardial injury and a high burden of pre-existing cardiovascular disease were significantly associated with higher mortality and ICU admission. [72]
• Lymphopenia is a common laboratory abnormality in most patients with COVID-19. Other laboratory abnormalities include thrombocytopenia, leukopenia, elevated ESR levels, C-reactive protein (CRP), lactate dehydrogenase (LDH), and leukocytosis.
• COVID-19 is also associated with a hypercoagulable state, evidenced by the high prevalence of venous thromboembolic events. COVID-19 is associated with markedly elevated D-dimer and fibrinogen levels and prolonged prothrombin time (PT) and partial thromboplastin time (aPTT). [71] [55]  
• GI symptoms (such as diarrhea, nausea, vomiting), anorexia, and abdominal pain are common. A meta-analysis reported that the weighted pool prevalence of diarrhea was 12.4% (95% CI, 8.2% to 17.1%), nausea or vomiting was 9% (95% CI, 5.5% to 12.9%), loss of appetite was 22.3% (95% CI, 11.2% to 34.6%) and abdominal pain was 6.2% (95% CI, 2.6% to 10.3%). The study also reported that the mortality rate among patients with GI symptoms was similar to the overall mortality rate. [73] Cases of acute mesenteric ischemia and portal vein thrombosis have also been described. [74]
• An acute increase in aspartate transaminase (AST) and alanine transaminase (ALT) is noted in 14% to 53% of patients with COVID-19 infection. [75]
• Guillain-Barré syndrome (GBS) cases from Northern Italy have also been reported. [76] [77]
• Acral lesions resembling pseudo chilblains (40.4%) are the most common cutaneous manifestation noted in patients with COVID-19. [78]
• Other cutaneous manifestations include erythematous maculopapular rash (21.3%), vesicular rashes (13%), urticarial rashes (10.9%), vascular rashes (4%) resembling livedo or purpura, and erythema multiforme-like eruptions (3.7%). [78]

Diagnostic Testing in COVID-19

A nasopharyngeal swab for SARS-CoV-2 nucleic acid using a real-time PCR assay is the standard diagnostic test.[ NIH COVID-19 Treatment Guidelines ] Commercial PCR assays have been authorized by the USA Food and Drug Administration (FDA) for the qualitative detection of SARS-CoV-2 virus using specimens obtained from nasopharyngeal swabs as well as other sites such as oropharyngeal, anterior/mid-turbinate nasal swabs, nasopharyngeal aspirates, bronchoalveolar lavage (BAL) and saliva. 

The sensitivity of PCR testing depends on multiple factors, including the specimen's adequacy, time from exposure, and specimen source. [79]  However, the specificity of most commercial FDA-authorized SARS-CoV-2 PCR assays is nearly 100%, provided there is no cross-contamination during specimen processing. SARS-CoV-2 antigen tests are less sensitive but have a faster turnaround time than molecular PCR testing. [80]  

Despite the numerous antibody tests designed to date, serologic testing has limitations in specificity and sensitivity, and results from different tests vary. According to the NIH guidelines, diagnosing acute SARS-CoV-2 infection based on serologic testing is not recommended. They also stated that there is insufficient evidence to recommend for or against using serologic testing to assess immunity, even if it is used to guide clinical decisions about COVID-19 vaccines/monoclonal antibodies.[ NIH COVID-19 Treatment Guidelines ]

Other Laboratory Assessment

• Complete blood count (CBC), a comprehensive metabolic panel (CMP) that includes renal and liver function testing, and a coagulation panel should be performed in all hospitalized patients.
• Additional tests, such as ESR, C-reactive protein (CRP), ferritin, lactate dehydrogenase, and procalcitonin, can be considered in hospitalized patients. However, their prognostic significance in COVID-19 is not clear.
• A D-dimer level is required as it guides the use of therapeutic versus prophylactic doses of anticoagulation.

Imaging ModalitiesThis s viral illness commonly manifests as pneumonia, so radiological imaging such as chest x-rays, lung ultrasounds, and chest computed tomography (CT) are often obtained. However, there are no guidelines regarding the timing and choice of pulmonary imaging in patients with COVID-19.

When obtained, the chest X-ray usually shows bilateral multifocal alveolar opacities. Pleural effusions can also be demonstrated. The most common CT chest findings in COVID-19 are multifocal bilateral ground glass opacities with consolidation changes, usually in a patchy peripheral distribution. [81]

Radiologic imaging is not a sensitive method for detecting this disease. A retrospective study of 64 patients with documented COVID-19 reported that 20% had no abnormalities on chest radiographs during the illness. [82]  A chest CT is more sensitive than a radiograph but is not specific. No finding on radiographic imaging can completely rule in or rule out COVID-19 illness. Therefore the American College of Radiology (ACR) advises against the routine use of chest CT for screening or diagnosis of COVID-19.[ ACR Position Statement for Diagnosis of COVID-19 ]

• Treatment / Management

According to the National Institutes of Health (NIH), the 2 main processes driving the pathogenesis of COVID-19 include replication of the virus in the early phase of the illness and dysregulated immune/inflammatory response to SARS-CoV-2 that leads to systemic tissue damage in the later phase of the disease.[ NIH COVID-19 Treatment Guidelines ] The guidelines, therefore, advise antiviral medications to halt viral replication in the early phase of the illness and immunomodulators in the later phase.

Remdesivir is the only antiviral drug approved by the USA Food and Drug Administration (FDA) to treat COVID-19. Ritonavir-boosted nirmatrelvir, molnupiravir, and high-titer COVID-19 convalescent plasma have Emergency Use Authorizations (EUAs) for treating COVID-19. Tixagevimab 300 mg plus cilgavimab 300 mg monoclonal antibodies have received EUAs that allow them to be used as SARS-CoV-2 preexposure prophylaxis (PrEP) in certain patients.

Many other monoclonal antibodies had EUAs; however, as Omicron subvariants emerged, their EUAs were revoked as they were no longer effective. 

The most recent NIH treatment guidelines for the management of COVID-19 illness (accessed on January 3rd, 2023) are outlined below:[ NIH COVID-19 Treatment Guidelines ]

Nonhospitalized Adults With Mild-to-Moderate COVID-19 Illness Who Do Not Require Supplemental Oxygen

• The NIH recommends against using dexamethasone or any other systemic corticosteroids in patients who are not hypoxic. [83]   
• Ritonavir-boosted nirmatrelvir is a combination of oral protease inhibitors. It has been shown to reduce hospitalization and death when given to high-risk, unvaccinated, nonhospitalized patients. It must be given within 5 days of symptoms onset. [84]
• It is a strong cytochrome P450 inhibitor with many drug-drug interactions that must be carefully assessed.
• Some interactions can be managed by temporarily holding the medication, some may be managed with dose adjustment, but some may warrant the use of alternate COVID-19 therapy. 
• Ritonavir-boosted nirmatrelvir is not recommended in patients with an estimated glomerular filtration rate (eGFR) of less than 30 mL/min.
• The recommended dose is nirmatrelvir 300 mg with ritonavir 100 mg orally twice daily for 5 days.
• This is a nucleotide analog that inhibits the SARS-CoV-2 RNA polymerase  
• The recommended duration of therapy in this setting is 3 days.
• The recommended dose is 200 mg IV on day 1, followed by 100 mg IV for 2 more days.
• It is a mutagenic ribonucleoside antiviral agent.
• Fetal toxicity has been reported in animal studies with this agent. Due to the risk of genotoxicity with this agent, it is not recommended in pregnant patients. 
• This agent should only be used if both therapies are unavailable or cannot be given.
• The NIH guidelines recommend against using anti-SARS-CoV-2 monoclonal antibodies (mAbs) for treating COVID-19 in this cohort because the Omicron subvariants are not susceptible to these agents.  
• Adequate and close medical follow-up is recommended; however, the frequency and duration of follow-up depend on individual risk factors and the severity of their symptoms. 
• Risk factors for progression to severe disease include advanced age and underlying medical conditions. The CDC maintains an updated list of medical conditions associated with a high risk of progression. 
•  Asthma
• Cerebrovascular disease
• Chronic kidney disease
• Bronchiectasis
• COPD (Chronic obstructive pulmonary disease)
• Interstitial lung disease
• Pulmonary embolism
• Pulmonary hypertension
• Nonalcoholic fatty liver disease
• Alcoholic liver disease
• Autoimmune hepatitis
• Cystic fibrosis
• Diabetes, type 1 and 2
• Heart conditions (such as heart failure, coronary artery disease, or cardiomyopathies)
• HIV (Human immunodeficiency virus)
• Mental health conditions such as mood disorders and Schizophrenia spectrum disorders
• Obesity (defined as body mass index (BMI) of greater than 30 kg/m 2 or greater than 95th percentile in children)
• Pregnancy and recent pregnancy
• Smoking, current and former
• Solid organ or blood stem cell transplantation
• Tuberculosis
• Use of corticosteroids or other immunosuppressive medications ( CDC: Underlying Medical Conditions Associated with Higher Risk )

Therapeutic Management of Hospitalized Adults With COVID-19   Who Do Not Require Oxygen

• If patients are hospitalized for reasons other than COVID-19 illness and are not on oxygen, their management is similar to nonhospitalized patients. 
• If they are hospitalized for COVID-19 illness but do not require oxygen, the NIH advises against the use of dexamethasone or any other systemic corticosteroid.
• A prophylactic dose of anticoagulation should be given if there is no contraindication. 
• If they are hospitalized for COVID-19 illness, do not require oxygen, but are at high risk of progression to severe disease, they should be treated with remdesivir.
• The benefit of remdesivir is greatest when given early, ideally within ten days of symptom onset.
• Remdesivir should be given for 5 days or until hospital discharge. 

Therapeutic Management of Hospitalized Adults With COVID-19 Who Require Conventional Oxygen

• Conventional oxygen is defined as oxygen that is NOT high-flow nasal cannula, noninvasive mechanical ventilation, mechanical ventilation, or extracorporeal membrane oxygenation (ECMO)
• For most patients in this cohort, the recommended treatment is dexamethasone plus remdesivir.
• Dexamethasone dose is 6 mg IV or oral (PO) once daily for up to 10 days or until hospital discharge (dexamethasone should not be continued at discharge). [83]  
• If the patient is on minimal oxygen, remdesivir monotherapy (without dexamethasone) should be used. 
• If remdesivir cannot be obtained or given, dexamethasone monotherapy is recommended.
• If dexamethasone is unavailable, corticosteroids such as prednisone, methylprednisolone, or hydrocortisone may be used.
• If the patient is already receiving dexamethasone but has rapidly increasing oxygen needs and/or signs of systemic inflammation, oral baricitinib or intravenous (IV) tocilizumab should be added to the treatment regimen as these agents have been shown to improve outcomes in rapidly decompensating patients. [85]
• Alternate immunomodulatory agents for this cohort include oral tofacitinib and IV sarilumab. These agents should only be used if baricitinib and tocilizumab are not available. 
• If the D-dimer level is above normal in this cohort of patients, they recommend therapeutic anticoagulation if the patient is not pregnant and has no increased risk of bleeding. Contraindications for therapeutic anticoagulation in these patients include a platelet count of less than 50 x10^9 /L, hemoglobin less than 8 g/dL, use of dual antiplatelet therapy, any significant bleeding within the past 30 days, a history of a bleeding disorder or an inherited or active acquired bleeding disorder. 
• For pregnant patients, a prophylactic dose of anticoagulation is recommended.

Therapeutic Management of Hospitalized Adults With COVID-19 who Require High-flow Nasal Cannula (HFNC) or Noninvasive Mechanical Ventilation (NIV)

• A meta-analysis study evaluating the effectiveness of HFNC compared to conventional oxygen therapy and NIV before mechanical ventilation reported that HFNC, when used before mechanical ventilation, could improve the prognosis of patients compared to conventional oxygen therapy and NIV. [86]  HFNC or NIV is associated with decreased dispersion of exhaled air, especially when used with good interface fitting, thus creating a low risk of nosocomial transmission of the infection. [87]  However, these treatment modalities are associated with a greater risk of aerosolization and should be used in negative-pressure rooms. [88]
• According to the NIH, dexamethasone plus oral baricitinib or dexamethasone plus IV tocilizumab are the preferred treatment regimens in these patients.
• Alternate immunomodulatory agents for this cohort include oral tofacitinib and IV sarilumab.
• Dexamethasone monotherapy is recommended if baricitinib, tocilizumab, or sarilumab cannot be obtained/given.
• Clinicians may consider adding remdesivir to corticosteroid and immunomodulator combination regimens in immunocompromised patients who require HFNC or NIV ventilation; however, using remdesivir without immunomodulators is not recommended.
• A prophylactic dose of anticoagulation is recommended in these patients. 
• If patients were started on a therapeutic dose of heparin while on conventional oxygen therapy, they should be switched to prophylactic dosing at this time unless they have another indication for full anticoagulation.

Therapeutic Management of Hospitalized Adults With COVID-19 who Require Mechanical Ventilation (MV)

• The management of this cohort is the same as those requiring HFNC or NIV, except that remdesivir is not recommended. 
• Remdesivir is most effective earlier in the course of the disease and in patients not on mechanical ventilation or ECMO.
• According to the NIH, one study showed a slight trend toward an increase in mortality in patients who received remdesivir while on mechanical ventilation or ECMO. [89]
• With this data in mind, the NIH recommends against using remdesivir in patients receiving MV or ECMO; however, if the patient was started on remdesivir and progressed to requiring mechanical ventilation or ECMO, they recommended continuing remdesivir to complete the treatment course. 

High-Titer COVID-19 Convalescent Plasma (CCP)

• The United States Food and Drug Administration (FDA) approved convalescent plasma therapy under a EUA for patients with severe life-threatening COVID-19. [90] [91]   Data from multiple studies evaluating the use of convalescent plasma in life-threatening COVID-19 has generated mixed results. Data from 3 small randomized control trials showed no significant differences in clinical improvement or overall mortality in patients treated with convalescent plasma versus standard therapy. [92] [93] [94]  
• According to the NIH, high-titer CCP is not recommended in immunocompetent individuals.
• However, the NIH states that some experts consider it appropriate for use in immunocompromised individuals. Therefore, the current NIH guidelines state that there is insufficient evidence for or against the use of high-titer CCP for treating COVID-19 in hospitalized or nonhospitalized patients who are immunocompromised.

Medications/Treatments That Should NOT Be Used for the Treatment of COVID-19 According to the Latest NIH Guidelines [ NIH COVID-19 Treatment Guidelines ]

• Chloroquine or hydroxychloroquine with or without azithromycin
• Lopinavir/ritonavir
• Azithromycin
• Doxycycline
• Fluvoxamine
• Inhaled corticosteroids
• Excess supplementation of vitamin C, vitamin D, and zinc
• Interferons alfa, beta, or lambda
• Nitazoxanide
• Bamlanivimab plus etesevimab
• Bebtelovimab
• Casirivimab plus imdevimab

Preexposure Prophylaxis for SARS-CoV-2 Infection

• According to the NIH guidelines, tixagevimab plus cilgavimab is authorized by the FDA for preexposure prophylaxis of SARS-CoV-2 in people who are not expected to mount an adequate immune response to COVID-19 vaccination; however, the prevalence of Omicron subvariants that are resistant to tixagevimab plus cilgavimab is noted to be increasing rapidly. 
• In the absence of alternative options, the NIH still recommends tixagevimab 300 mg plus cilgavimab 300 mg at this time.
• Tixagevimab and cilgavimab are potent anti-spike neutralizing monoclonal antibodies obtained from antibodies isolated from B cells of patients infected with SARS-CoV-2 that have demonstrated neutralizing activity against SARS-CoV-2 virus by binding to nonoverlapping epitopes of the viral spike-protein RBD. [95] [96] [97]  
• The EUA authorizes its use in adult and pediatric patients with no current evidence of SARS-CoV-2 infection and no recent exposure to SARS-CoV-2-positive individuals. They must be moderately or severely immunocompromised or be on immunosuppressive medications.
• Differential Diagnosis

The symptoms of the early stages of the disease are nonspecific. Differential diagnosis should include the possibility of a wide range of infectious and noninfectious respiratory disorders.

• Community-acquired bacterial pneumonia
• Viral pneumonia 
• Influenza infection
• Aspiration pneumonia
• Pneumocystis jirovecii pneumonia
• Middle East respiratory syndrome (MERS)
• Avian influenza A (H7N9) viral infection
• Avian influenza A (H5N1) viral infection
• Pulmonary tuberculosis

The prognosis of COVID-19 depends on various factors, including the patient's age, the severity of illness at presentation, preexisting conditions, how quickly treatment can be implemented, and response to treatment. The WHO currently estimates the global case fatality rate for COVID-19 is 2.2%. Results from a European multicenter prospective cohort study that included 4000 critically ill patients with COVID-19 reported a 90-day mortality of 31%, with higher mortality noted in geriatric patients and patients with diabetes, obesity, and severe ARDS. [98]

• Complications

COVID-19 is a systemic viral illness based on its involvement in multiple major organ systems.

• Patients with advanced age and comorbid conditions such as obesity, diabetes mellitus, chronic lung disease, cardiovascular disease, chronic kidney disease, chronic liver disease, and neoplastic conditions are at risk of developing severe COVID-19 and its associated complications. The most common complication of severe COVID-19 illness is progressive or sudden clinical deterioration leading to acute respiratory failure and ARDS or multiorgan failure leading to death.
• Patients with COVID-19 illness are also at increased risk of developing prothrombotic complications such as pulmonary embolisms, myocardial infarctions, ischemic strokes, and arterial thrombosis. [55]
• Cardiovascular system involvement results in malignant arrhythmias, cardiomyopathy, and cardiogenic shock.
• GI complications such as bowel ischemia, transaminitis, gastrointestinal bleeding, pancreatitis, Ogilvie syndrome, mesenteric ischemia, and severe ileus are often noted in critically ill patients with COVID-19. [99]
• Acute renal failure is the most common extrapulmonary manifestation of COVID-19 and is associated with an increased mortality risk. [69]
• A meta-analysis study of 14 studies evaluating the prevalence of disseminated intravascular coagulation (DIC) in hospitalized patients with COVID-19 reported that DIC was observed in 3% (95%: 1%-5%, P <0.001) of the included patients. Additionally, DIC was noted to be associated with severe illness and was a poor prognostic indicator. [100]
• More recent data have emerged regarding prolonged symptoms in patients who have recovered from COVID-19 infection, termed "post-acute COVID-19 syndrome." A large cohort study of 1773 patients performed 6 months after hospitalization with COVID-19 revealed that most exhibited at least one persistent symptom: fatigue, muscle weakness, sleep difficulties, or anxiety. Patients with severe illness also had an increased risk of chronic lung issues. [101]
• A retrospective cohort study that included 236,379 patients reported substantial neurological (intracranial hemorrhage, ischemic stroke) and psychiatric morbidity (anxiety disorder, psychotic disorder) 6 months after being diagnosed with COVID-19. [102]
• Secondary invasive fungal infections such as COVID-19-associated pulmonary aspergillosis and rhino-cerebro-orbital mucormycosis have increasingly been reported as complications in patients recovering from COVID-19. Risk factors for developing secondary fungal infection include comorbid conditions such as uncontrolled diabetes, associated lymphopenia, and excessive use of corticosteroids.
• Deterrence and Patient Education

The NIH COVID-19 Treatment Guidelines recommend COVID-19 vaccination as soon as possible for all eligible individuals. The CDC’s Advisory Committee on Immunization Practices (AI) determines eligibility eligibility. Four vaccines are authorized or approved in the United States to prevent COVID-19. According to the NIH guidelines, the preferred vaccines include:[ NIH COVID-19 Treatment Guidelines ]

• mRNA vaccine BNT162b2 (Pfizer-BioNTech)
• mRNA-1273 (Moderna)
• Recombinant spike protein with matrix-M1 adjuvant vaccine NVX-CoV2373 (Novavax)

The adenovirus vector vaccine Ad26.COV2.S (Johnson & Johnson/Janssen) is less preferred due to its risk of serious adverse events.[ NIH COVID-19 Treatment Guidelines ]

A primary series of COVID-19 vaccination is recommended for everyone older than 6 months in the United States. Bivalent mRNA vaccines that protect against the original SARS-CoV-2 virus strain and Omicron subvariants are recommended at least 2 months after receiving the primary vaccine series or a booster dose.[ NIH COVID-19 Treatment Guidelines ] 

• Enhancing Healthcare Team Outcomes

SARS-CoV-2 and its variants continue to cause significant morbidity and mortality worldwide. Prevention and management of this highly transmissible respiratory viral illness require a holistic and interprofessional approach that includes physicians' expertise across specialties, nurses, pharmacists, public health experts, and government authorities. There should be open communication among the clinical providers, pharmacists, and nursing staff while managing patients with COVID-19. Each team member should strive to keep abreast of the latest recommendations and guidelines and be free to speak up if they notice anything that does not comply with the latest tenets for managing COVID patients; there is no place for a hierarchy in communication that prohibits any team member from voicing their concerns. This open interprofessional approach will yield the best outcomes. 

Clinical providers managing COVID-19 patients on the frontlines should keep themselves periodically updated with the latest clinical guidelines about diagnostic and therapeutic options available in managing COVID-19, especially considering the emergence of new SARS-CoV-2 variants, which could significantly impact morbidity and mortality. Continued viral surveillance of new variants is crucial at regular intervals with viral genomic sequencing, given the possibility that more highly transmissible, more virulent, and treatment-resistant variants could emerge that can have a more catastrophic effect on global health in addition to the current scenario. A multi-pronged approach involving interprofessional team members can improve patient care and outcomes for this potentially devastating disease and help the world end this pandemic.

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• Cite this Page Cascella M, Rajnik M, Aleem A, et al. Features, Evaluation, and Treatment of Coronavirus (COVID-19) [Updated 2023 Aug 18]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

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How to Thrive as You Age

U.s. drops in new global happiness ranking. one age group bucks the trend.

Allison Aubrey

The U.S. ranks higher in the world happiness report when it comes to people aged 60 and older. Thomas Barwick/Getty Images hide caption

The U.S. ranks higher in the world happiness report when it comes to people aged 60 and older.

How happy are you? The Gallup World Poll has a simple way to gauge well-being around the globe.

Imagine a ladder, and think about your current life. The top rung, 10, represents the best possible life and the bottom rung, 0, represents the worst. Pick your number.

Researchers use the responses to rank happiness in countries around the globe, and the 2024 results have just been released.

This year, Finland is at the top of the list. Researchers point to factors including high levels of social support and healthy life expectancy, to explain the top perch of several Scandinavian countries.

Goats and Soda

Can a picture make you happy we asked photographers and here's what they sent us.

North America does not fare as well overall. As a nation, the United States dropped in the global ranking from 15th to 23rd. But researchers point to striking generational divides.

People aged 60 and older in the U.S. reported high levels of well-being compared to younger people. In fact, the United States ranks in the top 10 countries for happiness in this age group.

Conversely, there's a decline in happiness among younger adolescents and young adults in the U.S. "The report finds there's a dramatic decrease in the self-reported well-being of people aged 30 and below," says editor Jan-Emmanuel De Neve , a professor of economics and behavioral science, and the director of the Wellbeing Research Centre at Oxford University.

This drop among young adults is also evident in Canada, Australia and, to a lesser extent in parts of western Europe and Britain, too. "We knew that a relationship existed between age and happiness, but the biggest surprise is that it is more nuanced than we previously thought, and it is changing," says Ilana Ron-Levey , managing director at Gallup.

"In North America, youth happiness has dropped below that of older adults," Ron-Levey says. The rankings are based on responses from a representative sample of about 1,000 respondents in each country.

There are a range of factors that likely explain these shifts.

De Neve and his collaborators say the relatively high level of well-being among older adults is not too surprising. Researchers have long seen a U-shaped curve to happiness.

Children are typically happy, and people tend to hit the bottom (of the U) of well-being in middle age. By 60, life can feel more secure, especially for people with good health, financial stability and strong social connections. Living in a country with a strong social safety net can also help.

Shots - Health News

Can little actions bring big joy researchers find 'micro-acts' can boost well-being.

"The big pressures in life, [such as] having small children, a mortgage to pay, and work, have likely tapered off a bit," De Neve says. But what's so unexpected he says is the extent to which well-being has fallen among young adults.

"We would expect youth to actually start out at a higher level of well-being than middle-age individuals," De Neve says.

"People are hearing that the world is going to hell in a handbasket and the young especially are feeling more threatened by it," says John Helliwell , Professor Emeritus at the University of British Columbia, and a co-author of the study.

He says many younger people may feel the weight of climate change, social inequities, and political polarization which can all be amplified on social media.

But hope is not lost, Helliwell says.

He points to countries in eastern Europe where levels of well-being are on the rise among young people.

He says the older generations in the countries that make up the former Yugoslavia, tend to be less happy. "They are bearing the scars of genocide and conflict," he says.

But he says the younger people are looking beyond this history. "A new generation can put it in the past and think of building a better future and feel that they can be part of that," Helliwell says.

Stuck In A Rut? Sometimes Joy Takes A Little Practice

This story was edited by Jane Greenhalgh

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Guest Essay

One Way to Help a Journalism Industry in Crisis: Make J-School Free

By Graciela Mochkofsky

Ms. Mochkofsky is the dean at CUNY’s Craig Newmark Graduate School of Journalism.

Many uncertainties haunt the field of journalism today — among them, how we can reach our audience, build public trust in our work, and who is going to pay for it all. But one thing is certain: as complicated and dark as the world looks today, it would be much worse if journalists were not there to report on it.

Research shows that towns that have lost sources of local news tend to suffer from lower voter turnout, less civic engagement and more government corruption. Journalists are essential just as nurses and firefighters and doctors are essential.

And to continue to have journalists, we need to make their journalism education free.

This might sound counterintuitive given the state of the industry. Shrinking revenue and decreasing subscription figures have led to a record number of newsroom jobs lost. Much of the local news industry has fallen into the hands of hedge funds focused on squeezing the last drops of revenue out of operations by decimating them. Billionaires who appeared as saviors just a few years ago have grown tired of losing money on the media organizations they bought. Public trust in the value of news is at historical lows, while a growing percentage of people are avoiding the news altogether.

Generative artificial intelligence, which is on the verge of reshaping almost everything around us, is bringing yet another technological disruption to the industry. Against this grim backdrop, authoritarian leaders are increasingly targeting journalists as political enemies both at home and abroad.

And yet there are still tens of thousands of jobs in news media in America, with exceptional journalism being produced every day. Some major organizations have even found ways to thrive in the digital age. Prominent foundation leaders have started an effort to pour hundreds of millions of philanthropic dollars into local journalism, and a movement has formed to push for federal and local legislation to direct public funding to news. An initiative to replant local news has founded dozens of nonprofit newsrooms in cities around the country. And a small but growing number of organizations are redefining the way news agendas are set, focusing on rebuilding public trust within small communities.

No matter how the news industry evolves, we will continue to need journalists. Successful business models for media are necessary, but the most crucial element for strong, independent journalism is the people who make it. Given the present stakes in the industry, our society and the world, we need mission-driven, imaginative news leaders who are not bound by the models of the past, who have the motivation and freedom to reimagine the field, and the empathy and commitment to serve the public interest, undaunted by attacks and threats.

We must also move beyond the lack of economic and demographic diversity that has long been a problem in the industry. News has too often been reported by predominantly middle-class, white, male journalists, resulting in coverage that has repeatedly missed the issues that are most important to the people receiving the news, contributing to the public’s lack of trust in the media.

In a resource-starved industry, few newsrooms can offer the type of mentoring, guidance and time that it takes to shape a great journalist. This is now primarily the responsibility of journalism schools. It is the civic duty of these schools to find and train reporters and news leaders, instill in them an ethical foundation, help develop their critical thinking skills, allow them to try and fail in a safe environment, open doors and provide a support network. (Journalism schools should also contribute research in a variety of areas, from the impact of A.I. to new business models to identifying and responding to emerging threats.)

But the cost of a journalism education has become an insurmountable barrier for exactly the kind of people we need the most. And those who, with great effort, manage to overcome that barrier, carry a weight that could limit their professional options.

Reporters burdened with debt are less likely to take professional risks and more likely to abandon the field. According to the Bureau of Labor Statistics, the median reporter salary in America is less than $56,000 a year, or about $27 per hour. In low-income areas, where news deserts are more prevalent, annual salaries can be as low as $20,000. A Wall Street Journal report about the debt-to-income ratio of alumni of 16 journalism masters programs found that many graduates leave with debts that exceed their postgraduate income.

As the dean of the Craig Newmark Graduate School of Journalism at the City University of New York, I can tell you that half measures won’t solve this quandary. My school was founded in 2006 as a public alternative to elite journalism schools in the city and it remains one of the most affordable in the nation.

Our in-state students pay about a quarter of the cost of an equivalent degree from top-tier schools with which we successfully compete. This year alone, 90 percent of our students are on scholarships, and a record 25 percent are attending tuition-free. We also waived the $75 application fee this admission cycle and saw an increase of more than 40 percent in our applicant pool.

Thanks to these policies, we have succeeded where the media industry keeps failing. Over 50 percent of our students are people of color and from underserved communities. Many couldn’t have attended our school if we hadn’t offered significant scholarship support. But that’s not enough. Though we rank as one of the journalism schools with higher-medium-income and lower-median-debt alumni, our students still don’t graduate fully debt-free.

This is why this year, we began a campaign to go fully tuition-free by 2027. While other schools might face different financial challenges, we hope that many more will follow us.

We need journalists whose only obligations are to the facts and the society they serve, not to lenders; who are concerned with the public interest, not with interest rates; who can make risky decisions and take the difficult path if that’s what the mission requires, free of financial burden. Journalism schools can help achieve that. In tough times, it is natural to mourn the past or lament the present, but what we really need is bold action.

Graciela Mochkofsky is the dean at CUNY’s Craig Newmark Graduate School of Journalism. She is the author, most recently, of “ The Prophet of the Andes: An Unlikely Journey to the Promised Land .”

The Times is committed to publishing a diversity of letters to the editor. We’d like to hear what you think about this or any of our articles. Here are some tips . And here’s our email: [email protected] .

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