Category: Corona Virus

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Air pollution cost hundreds of lives during coronavirus pandemic – DutchNews.nl

April 4, 2024

April 3, 2024 Photo: Depositphotos.com

People who live in areas with poor air quality such as busy roads and factory farms are more likely to become infected with coronavirus and their symptoms are often more severe, leading to more hospitalisations and deaths, according to new Dutch research.

The results, the researchers say highlight the the importance of having cleaner air in the Netherlands, and offer insights for dealing with future pandemics.

The study, carried out by public health institute RIVM, Utrecht and Wagening universities and regional health boards, shows air pollution does not play a direct role in the process of spreading coronavirus.

But it does confirm other research that air pollution makes respiratory diseases worse.

The researchers looked at the first year of the epidemic, before people had been vaccinated, and found people who live in areas with relatively poorer air quality were more likely to become infected, end up in hospital or die.

Air quality can vary due to high volumes of traffic, industry and intensive livestock farming, the researchers said. In terms of coronavirus, livestock showed the most detrimental health effect.

In the period to 1 February 2021, around 22,500 people died from COVID-19, the report says. In the regions where the air quality was worse than the Dutch average, a total of 400 to 800 deaths could have been prevented if the air had been as clean as average. The cleaner the air, the greater the preventive effect.

Cleaner air would also have prevented 1,100 hospitalisations, the researchers said.

The outcomes of this study stress the importance of improving air quality in Europe, the report concluded. Moving toward the WHO air quality guidelines would improve health generally and reduce the impact of severe acute respiratory infections.

We could not provide the Dutch News service, and keep it free of charge, without the generous support of our readers. Your donations allow us to report on issues you tell us matter, and provide you with a summary of the most important Dutch news each day.

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Air pollution cost hundreds of lives during coronavirus pandemic - DutchNews.nl

Assessing Cardiac AEs and Remdesivir Efficacy in COVID-19 Hospitalized Patients – Physician’s Weekly

April 4, 2024

The following is a summary of Cardiac Adverse Events and Remdesivir in Hospitalized Patients with Coronavirus Disease 2019 (COVID-19): A Post Hoc Safety Analysis of the Randomized DisCoVeRy Trial, published in the March 2024 issue of Infectious Disease by Terzi et al.

Researchers started a retrospective study to assess the association between remdesivir and cardiac adverse events (AEs) in hospitalized COVID-19 patients receiving standard of care (SoC).

They utilized data from the DisCoVeRy trial involving hospitalized COVID-19 patients. They considered any initial AE within 29 days post-randomization in the modified intention-to-treat (mITT) group assigned to either remdesivir or control. They utilized Kaplan-Meier survival curves for analysis, calculating event rates using Kaplan-Meier estimates.

The results showed that cardiac AEs occurred in 11.2% of patients (46/410) in the remdesivir group and 11.3% of patients (48 /423) in the control group among the mITT population (n=833). No significant difference between the groups (HR 1.0, 95% CI 0.7-1.5, P=0.98), even when considering serious and non-serious cardiac AEs separately. Most reported events in both groups were arrhythmic (remdesivir: 84.8%, control: 83.3%) and had favorable outcomes. Occurrence of different cardiac AE subclasses, including arrhythmic events, did not significantly differ between the remdesivir and control groups (HR 1.1, 95% CI: 0.7-1.7, P=0.68).

Investigators concluded that remdesivir treatment did not increase the risk of cardiac adverse events in hospitalized moderate or severe COVID-19 patients compared to standard care, which aligns with other controlled trials and meta-analyses.

Source: academic.oup.com/cid/advance-article/doi/10.1093/cid/ciae170/7637630

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Assessing Cardiac AEs and Remdesivir Efficacy in COVID-19 Hospitalized Patients - Physician's Weekly

Rutgers University drops COVID-19 vaccine mandate: What you need to know – FOX 5 New York

April 4, 2024

NEW BRUNSWICK, N.J. - As of Monday, Rutgers University in New Jersey no longer requires students, faculty, staff, and university affiliates to get the COVID-19 vaccine.

Now reporting positive COVID-19 test results is not required at Rutgers.

In March 2021, Rutgers became the first in the nation to require COVID vaccination, and many higher-ed institutions followed.

RELATED: Rutgers University students, faculty, staff must get COVID vaccine booster

However, face masks are welcomed on campus, but aren't required.

Based on a recent survey conducted by the American College Health Association across 311 institutions, it was found that merely 7.4% persist in enforcing universal vaccination mandates for all students. Additionally, 10.7% of institutions mandate vaccination for specific subgroups, such as residential students, against coronavirus.

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Rutgers University drops COVID-19 vaccine mandate: What you need to know - FOX 5 New York

The Invisible Assault: How COVID-19 Clandestinely Ravages the Heart – SciTechDaily

April 4, 2024

A study finds that SARS-CoV-2 can cause heart damage indirectly through systemic inflammation, revealing a new understanding of cardiovascular complications from COVID-19 and suggesting potential anti-inflammatory treatments. Credit: SciTechDaily.com

NIH-supported research shows that the virus that causes COVID-19 can damage the heart without directly infecting heart tissue.

SARS-CoV-2, the virus that causes COVID-19, can damage the heart even without directly infecting the heart tissue, a National Institutes of Health-supported study has found. The research, published in the journal Circulation, specifically looked at damage to the hearts of people with SARS-CoV2-associated acute respiratory distress syndrome (ARDS), a serious lung condition that can be fatal. However, researchers said the findings could have relevance to organs beyond the heart and also to viruses other than SARS-CoV-2.

Scientists have long known that COVID-19 increases the risk of heart attack, stroke, and Long COVID, and prior imaging research has shown that over 50% of people who get COVID-19 experience some inflammation or damage to the heart. What scientists did not know is whether the damage occurs because the virus infects the heart tissue itself, or because of systemic inflammation triggered by the bodys well-known immune response to the virus.

This was a critical question and finding the answer opens up a whole new understanding of the link between this serious lung injury and the kind of inflammation that can lead to cardiovascular complications, said Michelle Olive, Ph.D., associate director of the Basic and Early Translational Research Program at the National Heart, Lung, and Blood Institute (NHLBI), part of NIH. The research also suggests that suppressing the inflammation through treatments might help minimize these complications.

To reach their findings, the researchers focused on immune cells known as cardiac macrophages, which normally perform a critical role in keeping the tissue healthy but can turn inflammatory in response to injury such as heart attack or heart failure. The researchers analyzed heart tissue specimens from 21 patients who died from SARS-CoV-2-associated ARDS and compared them with specimens from 33 patients who died from non-COVID-19 causes. They also infected mice with SARS-CoV-2 to follow what happened to the macrophages after infection.

In both humans and mice, they found the SARS-CoV-2 infection increased the total number of cardiac macrophages and also caused them to shift from their normal routine and become inflammatory.

When macrophages are no longer doing their normal jobs, which includes sustaining the metabolism of the heart and clearing out harmful bacteria or other foreign agents, they weaken the heart and the rest of the body, said Matthias Nahrendorf, M.D., Ph.D., professor of Radiology at Harvard Medical School and senior author on the study.

The researchers then designed a study in mice to test whether the response they observed happened because SARS-CoV-2 was infecting the heart directly, or because the SARS-CoV-2 infection in the lungs was severe enough to render the heart macrophages more inflammatory. This study mimicked the lung inflammation signals, but without the presence of the actual virus. The result: even in the absence of a virus, the mice showed immune responses strong enough to produce the same heart macrophage shift the researchers observed both in the patients who died of COVID-19 and the mice infected with SARS-CoV-2 infection.

What this study shows is that after a COVID infection, the immune system can inflict remote damage on other organs by triggering serious inflammation throughout the body and this is in addition to damage the virus itself has directly inflicted on the lung tissue, said Nahrendorf. These findings can also be applied more generally, as our results suggest that any severe infection can send shockwaves through the whole body.

The research team also found that blocking the immune response with a neutralizing antibody in the mice stopped the flow of inflammatory cardiac macrophages and preserved cardiac function. While they have yet to test this in humans, Nahrendorf said a treatment like this could be used as a preventive measure to help COVID-19 patients with pre-existing conditions, or people who are likely to have more severe outcomes from SARS-CoV-2 associated ARDS.

Reference: Virus-Induced Acute Respiratory Distress Syndrome Causes Cardiomyopathy Through Eliciting Inflammatory Responses in the Heart by Jana Grune, Geetika Bajpai, Pervin Tlin Ocak, Eva Kaufmann, Kyle Mentkowksi, Steffen Pabel, Nina Kumowski, Fadi E. Pulous, Kim A. Tran, David Rohde, Shuang Zhang, Yoshiko Iwamoto, Gregory R. Wojtkiewicz, Claudio Vinegoni, Ursula Green, Filip K. Swirski, James R. Stone, Jochen K. Lennerz, Maziar Divangahi, Maarten Hulsmans and Matthias Nahrendorf, 20 March 2024, Circulation. DOI: 10.1161/CIRCULATIONAHA.123.066433

Funding: This study was supported by NHLBI grants: HL139598, HL142494, HL155097, and HL149647.

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The Invisible Assault: How COVID-19 Clandestinely Ravages the Heart - SciTechDaily

How COVID-19 Treatments Affect Patients With IBD – Medscape

March 27, 2024

TOPLINE:

Inflammatory bowel disease (IBD) therapies for patients may need to be briefly halted during treatment for COVID-19, but it does not escalate IBD flares, with prior vaccination for COVID-19 helping reduce complications from the virus.

"Patients with IBD on advanced therapies were frequently treated for acute COVID-19. Although COVID-19 treatment was associated with temporary withholding of IBD therapy, it did not result in increased IBD flares," the authors wrote.

The investigation, led by Laura C. Sahyoun, MD, Section of Digestive Diseases, Yale School of Medicine, New Haven, Connecticut, was published online in Digestive Diseases and Sciences.

Owing to the small sample size, the outcomes comparing antivirals to intravenous antibodies and SARS-CoV-2 strain prevalence could not be assessed. This single-center study also may not reflect the different clinical practices pertaining to IBD and COVID-19 treatments.

The study did not receive any specific funding. One author reported receiving speaker fees and being part of advisory boards, and another author received research support and reported being a part of advisory boards.

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How COVID-19 Treatments Affect Patients With IBD - Medscape

COVID-19 Antibody Discovery Could Explain Long COVID – UVA Health Newsroom

March 27, 2024

UVA Healths Steven L. Zeichner, MD, PhD, and his team have made an antibody discovery that could explain some of the most perplexing mysteries about COVID-19 and long COVID.

UVA Health researchers have discovered a potential explanation for some of the most perplexing mysteries of COVID-19 and long COVID. The surprising findings could lead to new treatments for the difficult acute effects of COVID-19, long COVID and possibly other viruses.

Researchers led by UVAs Steven L. Zeichner, MD, PhD, found that COVID-19 may prompt some peoples bodies to make antibodies that act like enzymes that the body naturally uses to regulate important functions blood pressure, for example. Related enzymes also regulate other important body functions, such as blood clotting and inflammation.

Doctors may be able to target these abzymes to stop their unwanted effects. If abzymes with rogue activities are also responsible for some of the features of long COVID, doctors could target the abzymes to treat the difficult and sometimes mysterious symptoms of COVID-19 and long COVID at the source, instead of merely treating the downstream symptoms.

Some patients with COVID-19 have serious symptoms and we have trouble understanding their cause. We also have a poor understanding of the causes of long COVID, said Zeichner,a pediatric infectious disease expert at UVA Childrens. Antibodies that act like enzymes are called abzymes. Abzymes are not exact copies of enzymes and so they work differently, sometimes in ways that the original enzyme does not. If COVID-19 patients are making abzymes, it is possible that these rogue abzymes could harm many different aspects of physiology. If this turns out to be true, then developing treatments to deplete or block the rogue abzymes could be the most effective way to treat the complications of COVID-19.

Understanding COVID-19 Abzymes

SARS-CoV-2, the virus that causes COVID, has protein on its surface called the Spike protein. When the virus begins to infect a cell, the Spike protein binds a protein called Angiotensin Converting Enzyme 2, or ACE2, on the cells surface. ACE2s normal function in the body is to help regulate blood pressure; it cuts a protein called angiotensin II to make a derivative protein called angiotensin 1-7. Angiotensin II constricts blood vessels, raising blood pressure, while angiotensin 1-7 relaxes blood vessels, lowering blood pressure.

Zeichner and his team thought that some patients might make antibodies against the Spike protein that looked enough like ACE2 so that the antibodies also had enzymatic activity like ACE2, and that is exactly what they found.

Recently, other groups have found that some patients with long COVID have problems with their coagulation systems and with another system called complement. Both the coagulation system and the complement system are controlled by enzymes in the body that cut other proteins to activate them. If patients with long COVID make abzymes that activate proteins that control processes such as coagulation and inflammation, that could explain the source of some of the long COVID symptoms and why long COVID symptoms persist even after the body has cleared the initial infection. It also may explain rare side effects of COVID-19 vaccination.

To determine if antibodies could be having unexpected effects in COVID patients, Zeichner and his collaborators examined plasma samples collected from 67 volunteers with moderate or severe COVID on or around day 7 of their hospitalization. The researchers compared what they found with plasma collected in 2018, prior to the beginning of the pandemic. The results showed that a small subset of the COVID patients had antibodies that acted like enzymes.

While our understanding of the potential role of abzymes in COVID-19 is still in its early stages, enzymatic antibodies have already been detected in certain cases of HIV, Zeichner notes. That means there is precedent for a virus to trigger abzyme formation. It also suggests that other viruses may cause similar effects.

Zeichner, who isdeveloping a universal coronavirus vaccine, expects UVAs new findings will renew interest in abzymes in medical research. He also hopes his discovery will lead to better treatments for patients with both acute COVID-19 and long COVID.

We now need to study pure versions of antibodies with enzymatic activity to see how abzymes may work in more detail, and we need to study patients who have had COVID-19 who did and did not develop long COVID, he said. There is much more work to do, but I think we have made a good start in developing a new understanding of this challenging disease that has caused so much distress and death around the world. The first step to developing effective new therapies for a disease is developing a good understanding of the diseases underlying causes, and we have taken that first step.

Findings Published

The researchers havepublished their findings in the scientific journal mBio, a publication of the American Society for Microbiology. The research team consisted of Yufeng Song, Regan Myers, Frances Mehl, Lila Murphy, Bailey Brooks, and faculty members from the Department of Medicine, Jeffrey M. Wilson, Alexandra Kadl, Judith Woodfolk.

Its great to have such talented and dedicated colleagues here at UVA who are excited about working on new and unconventional research projects, said Zeichner.

Zeichner is the McClemore Birdsong Professor in the University of Virginia School of Medicines Departments of Pediatrics and Microbiology, Immunology and Cancer Biology; the director of the Pendleton Pediatric Infectious Disease Laboratory; and part of UVA Childrens Child Health Research Center.

The abzyme research was supported by UVA, including the Manning Fund for COVID-19 Research at UVA; the Ivy Foundation; the Pendleton Laboratory Fund for Pediatric Infectious Disease Research; a College Council Minerva Research Grant; the Coulter Foundation; and the National Institutes of Healths National Institute of Allergy and Infection Diseases, grant R01 AI176515. Additional support came from the HHV-6 Foundation.

To keep up with the latest medical research news from UVA, subscribe to theMaking of Medicineblog

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COVID-19 Antibody Discovery Could Explain Long COVID - UVA Health Newsroom

What’s Next for the Coronavirus? – Yahoo News

March 27, 2024

Rat droppings from New York City. Poop from dog parks in Wisconsin. Human waste from a Missouri hospital. These are some of the materials that are readying us for the next chapter of the coronavirus saga.

More than four years into the pandemic, the virus has loosened its hold on most peoples bodies and minds. But a new variant better able to dodge our immune defenses may yet appear, derailing a hard-won return to normalcy.

Scientists around the country are watching for the first signs.

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Were not in the acute phases of a pandemic anymore, and I think its understandable and probably a good thing that most people, including scientists, have returned to their pre-pandemic lives, said Jesse Bloom, an evolutionary biologist at the Fred Hutchinson Cancer Center in Seattle.

That said, the virus is still evolving; its still infecting large numbers of people, he added. We need to keep tracking this.

Bloom and other researchers are trying to understand how the coronavirus behaves and evolves as populations amass immunity. Other teams are probing the bodys response to the infection, including the complex syndrome called long COVID.

And some scientists have taken on an increasingly difficult task: estimating vaccine effectiveness in a crowded respiratory milieu.

Intellectually, this virus, to me at least, is only becoming more interesting, said Sarah Cobey, an evolutionary biologist at the University of Chicago.

In some ways, SARS-CoV-2 has been a fabulous reminder of some of the deepest questions in the field and also how far we have to go in answering a lot of them.

Closely analyzing new variants appearing in wastewater may help predict what additional forms may surface, said Marc Johnson, a virus expert at the University of Missouri, who has hunted for iterations of the coronavirus in stool samples from rodents and humans.

They help inform the evolution of this virus and whats likely to happen next, and possibly could even inform how to make a better vaccine, Johnson said.

The Black Swan Event

Evolutionary biology was once an esoteric pursuit involving humdrum hours staring at a computer screen. The works implications for public health were often tenuous.

The pandemic changed that. Vaccines can now be made more easily and much faster than before, so really understanding how viruses evolve has more and more practical utility, Bloom said.

Many evolutionary biologists who now study the coronavirus, including Bloom, were experts in influenza, which evolves into a new variant every two to eight years from its most immediate predecessor.

The scientists expected the coronavirus to behave similarly. But omicron arrived with dozens of new mutations a shocking black swan event, Bloom said. Then came BA.2.86, another huge jump in evolution, signaling that the virus remained unpredictable.

The iterations of a virus that thrive throughout a population have some sort of advantage an ability to sidestep the immune system, perhaps, or extreme contagiousness. In an individual, there is no such evolutionary pressure, said Katia Koelle, an evolutionary biologist at Emory University in Atlanta.

The result is that a chronic infection usually in an immunocompromised person offers the virus an opportunity to experiment with new formats, allowing it to hit the evolutionary equivalent of a fast-forward button. (Viral persistence in the body is also thought to play a role in long COVID.)

Chronic infections with the coronavirus are rare, even among immunocompromised people. But the alpha variant of late 2020, the omicron variant in late 2021 and BA.2.86, first detected in the summer of 2023 all are now thought to have emerged from immunocompromised people.

Some mutations acquired as the virus evolves may offer no benefit at all or may even hinder it, Koelle said. Not all of the virus versions pose a widespread threat to the population BA.2.86 ultimately did not, for example.

But these genetic alterations may nevertheless foreshadow the future.

After BA.2.86 emerged, close analysis of its genome revealed one spot where the virus remained sensitive to the bodys immune defenses. Johnson guessed that the virus next move would be to acquire a mutation in that very spot.

And sure enough, it just appeared, he said, referring to JN.1, the variant that now accounts for a vast majority of infections.

The more we see these lineages like BA.2.86, which appear to be from chronic infections, the more we have an argument like, hey, this really is something we should be paying attention to, he added.

Analyzing more than 20,000 samples of wastewater from across the country, Johnson has found fewer than 60 viral genetic sequences that are likely to be from immunocompromised people.

Such sequences turn up only when a super shedder an individual who sheds huge amounts of virus in their feces happens to live in an area with wastewater surveillance. Im sure there are a ton more out there, Johnson said. I just dont know how many more.

Spotty Surveillance

Scientists looking for signs of renewed danger are constrained by the limited surveillance for coronavirus variants in the United States and elsewhere.

Many countries, including the United States, ramped up tracking efforts at the height of the pandemic. But they have since been cut back, leaving scientists to guess the scale of respiratory virus infections. Wastewater and hospitalizations can provide clues, but neither is a sensitive measure.

We never have had especially systematic surveillance for respiratory pathogens in the United States, but its even less systematic now, Cobey said. Our understanding of the burden of these pathogens, much less their evolution, has been really compromised.

Not tracking viruses closely has another consequence: With multiple respiratory viruses to combat each year, it is now extremely challenging to gauge how effective the vaccines are.

Before COVID, scientists estimated the effectiveness of the influenza vaccine by comparing the vaccination status of those who tested positive for flu with those who did not.

But now, with vaccines for COVID and respiratory syncytial virus in the mix, the calculations are no longer simple. Patients turn up at clinics and hospitals with similar symptoms, and each vaccine prevents those symptoms to a different degree.

It becomes this much more complex network of prevention thats happening, said Emily Martin, a public health researcher at the University of Michigan. It does funny things to the numbers.

An accurate estimate of effectiveness will be crucial for designing each seasons vaccine, and for preparing doctors and patients to face a rough respiratory season.

In 2021, for example, the University of Michigan experienced an outbreak of influenza. When the researchers worked out that the seasons vaccine didnt protect against that strain, they were able to warn other college campuses to prepare for clusters in their dorms and hospitals to stock up on antiviral drugs.

Solving the problem may itself pose complications, because different divisions at the Centers for Disease Control and Prevention work on influenza, COVID and other respiratory diseases.

It requires problem-solving across these sort of artificial lines of different departments, Martin said.

Immunity and Long COVID

As coronavirus variant after variant materialized, it became clear that while the vaccines provided a powerful bulwark against severe illness and death, they were much less effective at stopping viral spread.

For a vaccine to prevent infections, it must induce antibodies not just in the blood, but at sites where the virus invades the body.

Ideally, youd want them across mucosal sites so, in your nose, in your lungs, said Marion Pepper, an immunologist at the University of Washington in Seattle.

Scientists discovered about 15 years ago that a large part of the bodys defenses comes not just from the cells and organs of the immune system, but from these other tissues.

One of the things that weve been really focused on is trying to understand immune responses in the tissues better than we did before, Pepper said.

In a small set of people, the virus itself may also persist in various parts of the body and may be one of the causes of long COVID. Vaccination and antiviral drugs alleviate some of the symptoms, lending credence to this idea.

At Yale University, Akiko Iwasaki and her colleagues are testing whether a 15-day course of antiviral drug Paxlovid can eliminate a slowly replicating reservoir of virus in the body.

Were hoping to get to the root cause if thats whats causing peoples illness, Iwasaki said.

She and her colleagues began studying immune responses to the coronavirus almost as soon as the virus appeared. As the pandemic progressed, the collaborations grew larger and more international.

And it became obvious that in many people, the coronavirus leaves a lasting legacy of immune-related problems.

Two years ago, Iwasaki proposed a new center to study the myriad questions that have arisen. Infections with many other viruses, bacteria and parasites also set off long-term complications, including autoimmunity.

The new virtual institute, started in the summer, is dedicated to studying post-infection syndromes and strategies to prevent and treat them.

Before the pandemic, Iwasaki was already busy studying viral infections with a big lab and multiple projects. But it doesnt begin to compare with her life now, she said.

Scientists tend to be obsessed about things that they work on, but not with this level of urgency, she said. Im pretty much working every waking hour.

c.2024 The New York Times Company

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What's Next for the Coronavirus? - Yahoo News

Pandemic course improved COVID-19 knowledge, study finds – Phys.org

March 27, 2024

This article has been reviewed according to ScienceX's editorial process and policies. Editors have highlighted the following attributes while ensuring the content's credibility:

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Early in the COVID-19 pandemic, more than 1,300 students enrolled in a three-week summer immersion course, "The Pandemic: Science and Society," at Washington University in St. Louis. The innovative course envisioned by Feng Sheng Hu, the Richard G. Engelsmann Dean of Arts & Sciences, brought together experts from across WashU and around the country.

A new study published in the journal Humanities and Social Sciences Communications examines the course's impact and implications for effective public health messaging for university students going forward.

Reviewing data submitted three months after the course concluded, researchers found a person's preferred information sources made a difference in their level of knowledge, risk perception and protective behaviors. People with higher COVID knowledge practiced more protective behaviors during the fall 2020 semester.

"We can emphasize the need for protective behaviors without causing a feeling of dread," said Krista Milich, an assistant professor of biological anthropology in Arts & Sciences who designed and taught the COVID-19 course. The pandemic course used such an approach to encourage safety behaviors while reiterating that those behaviors can make a difference.

"The course also created a sense of community during a time when many people were feeling isolated," Milich said.

The course was free to all full-time WashU students and ran from Aug. 17 to Sept. 4, 2020. Students from all WashU schools participated in online lectures and discussion boards, completed quizzes and created a piece of communicationeither a video, an infographic, a letter to the editor or a work of artabout the virus. Students shared their work on social media using the hashtag #COVIDcourse.

The new study analyzed data from nearly 1,000 anonymous questionnaires. The majority of respondents were WashU students (83%). About half of the respondents took the course, and another 26% had some exposure to course content, either by watching lectures online or hearing from others who attended.

Respondents said their top sources of COVID-19 information were family (52%), official health organization websites (50%), news media (47.4%), friends (38.6%) and the pandemic course (32.4%). Of these, health organizations and the course were associated with higher levels of COVID knowledge, more accurate risk perception and stronger protective behaviors.

"In our study, those who relied on social media had lower COVID knowledge scores and personal safety scores than those who relied on official sources," Milich said. Using friends or family as a primary source of information was also associated with lower COVID knowledge.

While the new analysis focuses on implications for future public health communication, the results indirectly point to a second success: WashU administrators largely achieved their goals for the course. Hu and other leaders hoped an immersive, interdisciplinary course would positively influence personal behaviors and improve compliance with recommended safety steps.

"I'm so pleased to see the positive impact the pandemic course had on our students and campus community," Hu said. "This course showcases two hallmarks of Arts & Sciencescollaboration and creativityand I hope it can serve as a model for other universities seeking to improve public health knowledge on campus."

The benefits of such a course are wide-reaching, Milich said. A university practicing safer behaviors can ultimately protect the larger community by preventing spillovers that could affect vulnerable individuals in the area.

"Our study illustrates how universities can design a curriculum to impact the behaviors of students during a pandemic, which will likely have positive impacts on the surrounding community," Milich said. "Providing reliable and accessible public health information may be an important way to reduce harm during future global health crises."

More information: Krista M. Milich et al, Effective public health messaging for university students: lessons learned to increase adherence to safety guidelines during a pandemic, Humanities and Social Sciences Communications (2024). DOI: 10.1057/s41599-023-02461-9

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Pandemic course improved COVID-19 knowledge, study finds - Phys.org

What’s Next for the Coronavirus? – The New York Times

March 27, 2024

Rat droppings from New York City. Poop from dog parks in Wisconsin. Human waste from a Missouri hospital. These are some of the materials that are readying us for the next chapter of the coronavirus saga.

More than four years into the pandemic, the virus has loosened its hold on most peoples bodies and minds. But a new variant better able to dodge our immune defenses may yet appear, derailing a hard-won return to normalcy.

Scientists around the country are watching for the first signs.

Were not in the acute phases of a pandemic anymore, and I think its understandable and probably a good thing that most people, including scientists, have returned to their prepandemic lives, said Jesse Bloom, an evolutionary biologist at the Fred Hutchinson Cancer Center in Seattle.

That said, the virus is still evolving, its still infecting large numbers of people, he added. We need to keep tracking this.

Dr. Bloom and other researchers are trying to understand how the coronavirus behaves and evolves as populations amass immunity. Other teams are probing the bodys response to the infection, including the complex syndrome called long Covid.

And some scientists have taken on an increasingly difficult task: estimating vaccine effectiveness in a crowded respiratory milieu.

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What's Next for the Coronavirus? - The New York Times

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