Covid causes influenza and other common viruses to act in unfamiliar ways

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At one point last month, children were admitted to Yale New Haven Children’s Hospital with a staggering range of seven respiratory viruses. They had adenovirus and rhinovirus, respiratory syncytial virus and human metapneumovirus, influenza and parainfluenza, as well as coronavirus, which many experts say is to blame for the unusual jumps.

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

More than two years after the coronavirus pandemic, known viruses act in an unknown way. The respiratory syncytial virus, known as RSV, usually 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 return in December after not appearing a year ago, disappeared again in January after the omicron variant of the coronavirus became necessary. Now the flu is back, but without a common line known as the Yamagata, which has not been seen since early 2020. It may have disappeared or may be waiting to attack our unsuspecting immune system, researchers said.

Follow-up of coronavirus cases

The concussion is felt in hospitals and laboratories. Doctors are rethinking routines, including holding preventive vaccines in the spring and even summer. Researchers have a rare opportunity to understand whether changes in behavior such as orders to stay at home, disguise and social distance are responsible for viral changes and what evolutionary advantage SARS CoV-2 may have over its microscopic rivals.

“This is a massive natural experiment,” said Michael Mina, an epidemiologist and chief research officer at the eMed digital health platform. Mina said that 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 correcting protocols that for decades reflect a predictable cycle of diseases that come and go when schools close or change.

“You’ll see a child with a fever and think, ‘What time of year is it?'” Said Peter Hotez, a molecular virologist and dean of the National School of Tropical Medicine at Baylor College of Medicine in Houston.

For years, Teresa Barton, head of pediatric infectious diseases at the University of San Antonio Health, routinely supported the flu vaccine each fall and weakened her advocacy until March and April, when the flu disappeared. The new change in seasonality, with an increase in flu cases last summer and then again this spring, has made her rethink.

You’re like “Oh, man!” In clinics. “Let’s get you a flu shot,” Barton said.

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She and other infectious disease specialists are also reviewing their response to RSV, a common virus that hospitalizes about 60,000 children under the age of five each year, according to the Centers for Disease Control and Prevention. It can cause deadly lung infections in premature and other high-risk babies. The typical treatment for them is monthly injections of a monoclonal antibody, palivizumab, from about November to February. But last summer, the RSV rose sharply, and this year is causing problems in May and June. Infectious disease experts are closely monitoring cases to be ready to reactivate the expensive protocol.

“We’re monitoring the number of cases, so if it exceeds a number, we’re ready,” Murray said. Yale Hospital, which usually holds meetings to prepare for the rise in the fall to spring, is preparing pandemic-weary employees for off-season jumps.

Even the common cold seems a little more virulent and persistent, according to Richard Martinello, a specialist in respiratory viruses at Yale Medical School.

“When people get colds, they seem to be a little worse,” he said, stressing that the evidence so far has been largely anecdotal.

The changes – and how and when they can 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 along with pathogens, and our regular contact with them usually allows our immune system to resume the reaction without making us very ill.

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

The moment you stop seeing the virus in that regular rhythm, as happened during the pandemic, that natural balance is upset, Mina said. The extraordinary measures we have taken to limit coronavirus exposure – necessary steps to control a new deadly enemy – have also limited our exposure to other viruses. However, if you are exposed to the virus after too much time, you may not be able to defend yourself, leading to off-season jumps in the population and surprisingly virulent infections for individuals.

Mina and others say it happened after people took off their masks and began to gather indoors. The viruses began to circulate out of season, as population immunity was low, even if other conditions were not optimal for them.

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

The same process of immune memory is already well documented by other phenomena, Mina said, similar to 35- and 40-year-olds who get shingles, reactivation of the chickenpox virus, which usually affects the elderly or people with weakened immune systems.

Before the advent of chickenpox vaccines, people were usually infected as children and then had a series of natural intensifying events throughout their lives, restarting their immunity when they came in contact with infected friends and then with their own children and friends. your children.

Now that these children are protected, they do not provide their parents with these natural stimuli, making these adults vulnerable to the herpes zoster virus again.

This phenomenon will be short-lived, as younger people who are protected by the chickenpox vaccine are aging and will not be at risk of getting shingles.

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

It is not yet clear whether the decline in influenza cases in January, for example, was caused entirely by people withdrawing from each other with the spread of omicron, or whether the coronavirus acted to repel its more common rival by some means. another mechanism.

“It’s a wonderful question whether omicron pushed it out,” said Xiaoyang Song, chief infection control specialist at the Children’s National Hospital in the area. Even more mysterious is the role that Kovid played in removing Yamagata from the game. When the flu returned this spring, that line was nowhere to be found.

Ellen Foxman, an immunobiologist at Yale School of Medicine, has spent years researching how viruses interact and what genetic and environmental factors mean that the same virus can cause colds in one person and cause serious illness in another.

It is a high-tech plant that uses nasal and lung cells to grow human airway tissue in the laboratory before infecting it with viruses, along with environmental pollutants such as cigarette smoke.

The study of the nasal mucosa gave an idea of ​​what is known as innate immunity. Once these cells detect a virus, they turn on antivirus protection by blocking other viruses. This process may help explain why the long-awaited twindemia of coronavirus and other viruses, possibly hampered by remote work and camouflage in the winter of 2020 to 2021, has not yet occurred this past winter, despite sporadic co-infections.

The cohort of babies born in the last two years will provide a lot of information. Usually a child under the age of 5 has an average virus in his nose 26 out of 50 weeks a year. Serious RSV and rhinovirus infections in 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 their lung development,” Foxman said, making them key to understanding the link between the viral infection and asthma.

However, it is not clear what the future holds, as the covid settles among us.

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

Mina expects that the coronavirus, like other respiratory viruses, will fall into a pattern of seasonal circulation as the population’s immunity increases, reducing what is known as the “force of infection.”

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

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

Despite these continuing uncertainties, for many researchers, the cataclysms caused by the pandemic have reinforced some strategies to prevent infection.

Scott Hensley, a microbiologist at Perelman School of Medicine at the University of Pennsylvania, is not convinced that the Yamagata flu is gone forever. It can still circulate, unnoticed, at very low levels, he said, ready to return to the stage. However, there is a proven method of protection – through vaccination.

“Even in years when vaccines don’t match, there’s a certain level of protection,” Hensley said, “preventing hospitalizations and deaths.”

For Foxman, the laboratory scientist, the silver line of the pandemic was the way it would advance in science.

Although he continues to invest in high-tech experiments in his lab, Foxman says the biggest lesson the pandemic has taught her is to stop the spread of viral infections comes from simple behavioral changes, such as camouflage, which she says should continue. in strategic circumstances.

“We need to share some of the lessons we learned,” Foxman said.

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