Covid makes flu and other common viruses act in unknown ways

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At some point last month, children were admitted to Yale New Haven Children’s Hospital with a startling array of seven respiratory viruses. They had adenovirus and rhinovirus, respiratory syncytial virus and human metapneumovirus, influenza and parainfluenza, as well as coronavirus – which many specialists believe is the cause of the unusual outbreaks.

“It’s not typical at any time of the year and certainly not typical in May and June,” said Thomas Murray, an infection control expert and associate professor of pediatrics at Yale. Some children admitted to hospital have been co-infected with two viruses and a few with three, he said.

More … than two years into the coronavirus pandemic, familiar viruses are acting in unknown ways. The respiratory syncytial virus, known as RSV, generally limits its choking attacks to the winter months.

Rhinovirus, the cause of the common cold, rarely sends people to the hospital.

And the flu, which seemed to be making a comeback in December after being absent the previous year, disappeared again in January once the omicron variant of the coronavirus took hold. Now the flu is back but without a common lineage known as Yamagata, which hasn’t been spotted since early 2020. It could have died out or waited to attack our unsuspecting immune systems, researchers said.

Coronavirus case tracking

The upheaval is felt in hospitals and laboratories. Doctors are rethinking routines, including keeping preventative injections on hand in the spring and even summer. Researchers have a rare opportunity to determine whether behavioral changes such as stay-at-home orders, masking and social distancing are responsible for viral changes, and what evolutionary advantage SARS CoV-2 may exert over its microscopic rivals. .

“It’s a massive natural experiment,” said Michael Mina, epidemiologist and scientific director of digital health platform eMed. Mina said the change in seasonality is largely due to our lack of recent exposure to common viruses, which makes us vulnerable to their return.

In hospitals across the country, doctors are adjusting protocols that for decades reflected a predictable cycle of illnesses that came and went as schools closed or the weather changed.

“You would see a child with a feverish illness and you would think, ‘What time of year is it?’ said Peter Hotez, molecular virologist and dean of the National School of Tropical Medicine at Baylor College of Medicine in Houston.

For years, Theresa Barton, head of pediatric infectious diseases at University Health San Antonio, regularly advocated for the flu vaccine each fall and eased her advocacy in March and April when the flu died down. The new change in seasonality, with the increase in flu cases last summer, then this spring, made it rethink.

“You’re like, ‘Oh man!’ in clinics. “Let’s get the flu shot,” Barton said.

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She and other infectious disease specialists are also re-examining their response to RSV, a common virus that hospitalizes about 60,000 children under age 5 each year, according to the Centers for Disease Control and Prevention. It can create fatal lung infections in premature babies and other high-risk infants. Typical treatment for them is monthly injections of a monoclonal antibody, palivizumab, from around November to February. But last summer the RSV suddenly increased and this year it is causing problems in May and June. Infectious disease experts are carefully monitoring cases to be ready to reactivate the costly protocol.

“We are monitoring the number of cases so that if it goes above a certain number, we are ready,” Murray said. Yale Hospital, which typically holds meetings to prepare for fall-to-spring surges, is preparing pandemic-weary staffers for off-season surges.

Even colds seem a bit more virulent and tenacious, according to Richard Martinello, a respiratory virus specialist at Yale School of Medicine.

“When people catch a cold, they seem a little worse,” he said, pointing out that so far the evidence is largely anecdotal.

The changes – and how and when they may return to normal – reflect changes in our own behavior during the pandemic as well as the interaction between SARS CoV-2 and other viruses, known as viral interference.

We have evolved alongside pathogens, and our regular contact with them usually allows our immune system to kick-start the response without making us very sick.

The system has “enough memory to make it more of a good hearty booster than a bad infection,” Mina said.

The moment you stop seeing a virus at that regular rate, as has happened during the pandemic, that natural balance is upset, Mina said. The extraordinary measures we have taken to limit exposure to the coronavirus – measures necessary to contain a deadly new enemy – have also limited our exposure to other viruses. If you are exposed to a virus again after too much time has passed, you may not be able to protect yourself as well, leading to off-season surges in the population and surprisingly virulent infections for individuals.

According to Mina and others, that’s what happened once people took off their masks and started congregating indoors. Viruses started circulating out of season because population immunity was low even though other conditions for them were not optimal.

“All of these decisions have consequences,” Murray said. “You do the best you can with the information you have.”

The same immune memory process is already well-documented by other phenomena, Mina said, such as 35- and 40-year-olds who contract shingles, a reactivation of the chickenpox virus that typically affects older people or people whose immune system immune is weakened.

Before the advent of varicella vaccines, people were typically infected in childhood and then went through a series of natural reinforcing events throughout their lives, rebooting their immunity upon contact with infected friends and then their own. children and friends of their children.

Now that these children are protected, they are not providing their parents with these natural stimulants, again making these adults vulnerable to the virus in the form of shingles.

This will be short-lived, as young people who are protected by the varicella vaccine grow older and are not at risk of getting shingles.

While vaccines disrupt the viral landscape by limiting the spread of infections, during the pandemic an entirely new virus – SARS Cov-2 – does so by interacting with its more common rivals.

It is not yet clear whether the drop in flu cases in January, for example, was entirely caused by people moving further apart as the omicron spread or whether the coronavirus acted to spread its most common rival through another mechanism.

“It’s a wonderful question whether omicron pushed it,” said Xiaoyan Song, infection control officer at the district’s National Children’s Hospital. Even more mysterious is the role covid played in putting Yamagata out of action. When the flu returned this spring, this line was nowhere to be found.

Ellen Foxman, an immunobiologist at the Yale School of Medicine, has spent years exploring how viruses interact and what genetic and environmental factors mean the same virus can cause a cold in one person and make another very sick.

It’s a high-tech company that uses nose and lung cells to grow human airway tissue in the lab before infecting it with viruses, as well as environmental contaminants like cigarette smoke.

Studying the lining of the nasal passages has provided insight into what is called innate immunity. Once these cells detect a virus, they activate antiviral defenses, blocking other viruses. This process may help explain why the long-awaited twin outbreaks of the coronavirus and other viruses, likely inhibited by remote working and masking in the winter of 2020 to 2021, still did not occur last winter. despite sporadic co-infections.

The cohort of babies born in the past two years will provide a lot of information. Normally, a child under the age of 5 has an average virus in the nose 26 out of 50 weeks of the year. Severe RSV and rhinoviruses infections during these early years are associated with the development of asthma later in life.

“These children did not have an infection at a crucial time in lung development,” Foxman said, making it key to understanding the relationship between viral infection and asthma.

Yet, we do not know what the future holds for us, as the covid takes hold among us.

“It will take time and even years to see what the new balance will look like,” Martinello said.

Mina predicts that the coronavirus, like other respiratory viruses, will fall into a seasonal circulation pattern once population immunity increases, decreasing what is known as the “strength of infection.”

“When you have a lot of people who don’t have immunity, the impact of the season is less. It’s like an open field,” Mina said. The virus “can overcome seasonal barriers.”

All of these changes will be affected by other environmental factors, Barton says, as climate change alters seasonal weather patterns.

Despite these lingering uncertainties, for many researchers, the upheaval caused by the pandemic has reinforced known strategies for preventing infection.

Scott Hensley, a microbiologist at the University of Pennsylvania’s Perelman School of Medicine, isn’t convinced the Yamagata flu is gone forever. It can still circulate, undetected, at very low levels, he said, ready to return to the scene. Yet there is a proven method to protect us – through vaccination.

“Even in years when the vaccines don’t match, there is some level of protection,” Hensley said, “preventing hospitalizations and deaths.”

For Foxman, the lab scientist, the silver lining of the pandemic has been how it will advance science.

Although she continues to invest in high-tech experiments in her lab, Foxman says the biggest lesson the pandemic has taught her about stopping the spread of viral infections comes from simple behavioral changes, like masking. , which she says should be pursued strategically. terms.

“We need to continue some of the lessons we’ve learned,” Foxman said.

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