Tag Archives: Coronaviridae

Health

Can Being Cold Really Give You a Cold?

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Photo: Olesia Bilkei (Shutterstock)

Kids never seem to want to dress appropriately for any occasion—or at least mine don’t. They want to wear pajamas to school, halloween costumes to bed, and summer clothes when it’s snowing out. So we say what we need to say to get them to put their hats on, right? “You’ll catch your death of cold!”

But can you really catch a cold from cold weather? Colds are caused by viruses, so no. But can cold weather make you more susceptible to those viruses? Well, that’s a little more complicated. But probably still no.

Colds are caused by viruses

Colds are infectious diseases caused by germs—specifically viruses. So, no, chilly weather cannot cause a cold all by itself. There is more than one virus that can cause a cold, though. A “cold” is just a word we use to describe a group of symptoms that occur with common respiratory viruses: sore throat, runny nose, coughing, sneezing. According to the CDC, some of the viruses that cause colds include:

  • rhinoviruses
  • adenoviruses
  • respiratory syncytial virus (RSV)
  • coronaviruses (not counting COVID and SARS, even though they are also coronaviruses)
  • human parainfluenza viruses
  • human metapneumoviruses

Because colds spread from person to person, to avoiding catching one the CDC recommends washing your hands, not touching your face with unwashed hands, and avoiding close contact with people who are sick. Putting a hat on when you go outside is not on the list of preventive measures.

Why are colds more common in winter?

The idea that colds can cause a cold may have arisen from the observation that colds are more common in the winter. But a lot of things are different in winter than in summer that affect the spread of respiratory viruses.

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For one, we tend to stay inside when it’s cold out, and this puts us into closer contact with others. Cold viruses spread more easily this way—just like COVID does.

Another factor is that cold air carries less moisture than warm air. That means the mucous membranes inside our noses can dry out more easily, whether we’re in the cold weather outside or in dry warm air indoors. (That warm air is often just the cold, dry air from outside, warmed up.) Those membranes are part of our defenses against viruses, so the dry air may make us more susceptible to colds.

There are still more hypotheses for why respiratory viruses, including colds and flu, are more common in winter. One is that we get less sunlight and thus less vitamin D. Another is that the viruses may survive longer outside the body when the weather is cold. Some proponents of the “cold makes you catch a cold” myth like to point out that being cold can stress your body, and any stress can potentially affect your immune system. While this is true, it seems unlikely to be much of a factor in whether or not you come down with a cold.

What about William Henry Harrison?

That probably all makes sense, but what about William Henry Harrison, our ninth president, the one who served for barely a month? As the history books tell us, he wanted to make a big deal about how hale and hearty he was, so he gave a long inauguration speech while standing in the cold sans hat or coat. He caught a cold as a direct result of that, it developed into pneumonia, and he died. So how is that possible?

First off, it’s worth being suspicious of that story because of how neat and convenient it seems. The man died because of the consequences of his own hubris. Great story. But did he really catch a cold, and was it really because of the hatless speech? According to a reexamination of the evidence in a 2014 issue of the journal Clinical Infectious Diseases, the answer to both questions is probably no.

Harrison definitely didn’t catch a cold after his speech. He only started feeling unwell three weeks later. His symptoms in the first few days were a headache, abdominal pain, and constipation, along with a fever. A cough appeared later, a few days before he died. So why does everybody think he died of pneumonia? His doctor was puzzled by the president’s collection of symptoms, the authors of the 2014 analysis wrote, yet had to give an answer that would make sense to the public:

In response to intense pressure from a stunned public to provide an explanation for the loss of their newly elected leader, he gave them pneumonia as his answer, though with obvious reservations. “The disease was not viewed as a case of pure pneumonia [he wrote]; but as this was the most palpable affection, the term pneumonia afforded a succinct and intelligible answer to the innumerable questions as to the nature of the attack”

But the authors note that the president’s gastrointestinal symptoms were more severe than his respiratory ones, and that it’s likely he died of “enteric fever”—or to put that in simpler terms, a really bad stomach bug (possibly typhoid).

Washington, D.C. did not have a sewer system at the time, and the White House’s water supply was suspiciously close to one of the city’s dumping grounds for human waste. The authors point out that presidents James Polk and Zachary Taylor also had episodes of severe gastrointestinal illness while living in the White House during this era (Taylor also died of it). But, sure, let’s blame Harrison for not wearing a hat in the cold.

   

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Health

Italian Man With Fever Learns He Has Monkeypox, Covid-19, and HIV All at Once

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An example of monkeypox rashes.
Image: Shutterstock (Shutterstock)

A 36-year-old man in Italy appears to be uniquely unlucky, after he was hospitalized and diagnosed with covid-19, monkeypox, and HIV over a span of a single week in July. Thankfully, his covid and monkeypox co-infections did successfully clear up without issue, and he has since been placed on HIV treatment.

His doctors describe this unfortunate medical tale in a case report published last week in the Journal of Infection. According to the report, the man first became ill with a fever, sore throat, and headache on June 29, nine days after having returned from a trip to Spain. On July 2, he tested positive for the SARS-CoV-2 coronavirus, but that same day, he also noticed a rash starting to develop on his left arm. Over the next few days, the rash turned into small, painful blisters that spread along his face, torso, lower limbs, and glutes. On July 5, he sought care at the emergency department of a local hospital in Catania, Italy, where he was then admitted into the infectious disease unit.

Given the man’s symptoms and recent travel to Spain, doctors quickly suspected monkeypox infection and collected samples for testing (the country was one of the first to report cases this year). While in Spain, the man also reported having condomless sex with other men, which has been a risk factor for monkeypox during the current outbreak. Finally, on July 6, the man tested positive for monkeypox, HIV, and the coronavirus—specifically, the Omicron BA.5.1 variant.

“To date, no reports of co-infection with monkeypox virus and SARS-CoV-2 have been published,” the authors wrote. “Therefore, in this study we present the clinical features and diagnostic procedure of the first documented case of co-infection with monkeypox virus, SARS-CoV-2, and HIV-1.”

Due to their respective incubation periods, the man could have caught the coronavirus and monkeypox at the same time. It’s thought to take anywhere from three to 17 days after exposure for monkeypox symptoms to appear, and around two to 14 days for covid-19 symptoms to show up (though the incubation period has likely gotten shorter on average for Omicron). As for the HIV infection, the man told doctors that he tested negative for it in September 2021. And since his CD4 lymphocyte count was still normal, it’s likely that this infection was caught recently as well. It can take 10 to 90 days following exposure to test positive for HIV, depending on the test used, and early flu-like symptoms may appear within a few weeks to a month.

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Though co-infections can sometimes contribute to more severe illness, it’s not clear whether that played any role in this case. By day three of the man’s hospitalization, most of his rashes started to crust over; by day five, his symptoms had almost completely resolved and he was sent home soon after. By July 13, he was no longer testing positive for the coronavirus, and on July 19, a follow-up visit to the doctors revealed that his crusty rashes had healed over almost completely, though he was still positive for monkeypox on a swab test. He was also started on a standard combination therapy for HIV, which is known to be very effective at keeping the chronic infection at bay when taken regularly.

While monkeypox may be able to spread to others through any kind of prolonged close contact, evidence continues to show that the vast majority of cases during this outbreak have been transmitted during sex, and most often among gay and bisexual men who have had multiple recent partners—perhaps both from close contact with contagious rashes and through infectious semen or other bodily fluids. Because the covid-19 pandemic is still ongoing and monkeypox cases are on the rise, the authors say that doctors should be aware of the possibility of co-infection in high-risk groups. They also add that their case emphasizes the predominant role that sex could be having in spreading monkeypox.

“Therefore, complete STI screening is recommended after a diagnosis of monkeypox,” they wrote.

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Vast Majority of Long Covid Patients Were Never Hospitalized, Report Finds

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Photo: Sirachai Arunrugstichai (Getty Images)

The average person suffering from long covid didn’t have a severe infection to begin with, a new report suggests. The study, an examination of private insurance claims, found that three-fourths of diagnosed long covid patients were not hospitalized for covid-19. Additionally, the researchers found that patients were most likely to be co-diagnosed with symptoms such as fatigue and trouble breathing.

Last October, long covid was codified into the latest edition of the International Classification of Disease (ICD-10), a codebook used by doctors, hospitals, and insurance companies for diagnostic and billing purposes. This code, officially known as “U09.9 Post covid-19 condition, unspecified,” allowed patients to be formally recognized as having long covid. But it also provided another way for researchers to study these patients on a larger scale.

This report, conducted by FAIR Health, a nonprofit company that describes itself as having the country’s largest database of privately billed health insurance claims, is one of the first pieces of research to do just that.

Using their database, the authors identified nearly 80,000 patients who had been diagnosed with post-covid symptoms in the four months after the ICD code was implemented, up through January 2022. Most patients (75.8%), they found, had never been hospitalized for their original covid-19 case.

“Post-covid conditions have become an issue of growing national concern,” said Robin Gelburd, FAIR Health president, in a news release. “We hope these findings prove helpful for all individuals diagnosed with post-covid conditions, as well as for providers, payors, policy makers and researchers.”

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Other research has consistently found that the more severe your initial infection, the more likely you are to experience lingering complications and early death. But studies have also shown that even people with mild to moderate cases are at risk for developing a variety of health problems afterward, to a greater extent than people who experience other respiratory infections. Most people who catch covid-19 also don’t end up in the hospital. So while the individual risk of prolonged symptoms may be smallest for people who had milder covid-19, there are simply many more people in that group than there are survivors of severe illness.

The report’s other findings might provide added insight into long covid. The most represented age group of patients (34.6%) were between 36 and 50 years old, for instance, but that might be because older Americans are usually covered through public Medicare plans. Women were more likely to be diagnosed than men and were more likely to not have been hospitalized originally. The three most common conditions to be diagnosed at the same time were “abnormalities of breathing” (23.2%), cough (18.9%), and malaise/fatigue (16.7%). And while many patients did have preexisting health conditions, 30% had been never diagnosed with any chronic illness prior to their long covid.

The report is a white paper, meaning that it hasn’t gone through formal peer review, an important part of validating any scientific research. So the findings should be taken with more caution than usual. No single study, even peer-reviewed, should be the final word on anything. But the sheer amount of data available does lend credibility to the results, and it’s likely that other researchers will be able to use ICD-10 data for similar studies in the future.

For their part, the authors do plan to analyze their data further, both to track the long-term outcomes of these patients and to examine whether vaccination reduced the risk of long covid, as other research has suggested it can.

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Experimental Nasal Spray Could Provide Temporary Protection Against Covid-19

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A transmission electron micrograph of SARS-CoV-2 virus particles (in gold) within endosomes of a heavily infected nasal olfactory epithelial cell.
Photo: NIH/NAID/IMAGE.FR/BSIP/Universal Images Group (Getty Images)

Researchers in Finland say they’ve created a novel nasal spray treatment that can provide brief but effective protection from the coronavirus and its many variants, including Omicron. In a recent preliminary study of cells in a petri dish as well as mice, the nasal spray appeared to block the virus from infecting cells up to eight hours following a dose. But more research would have to be done before we could expect this therapy to reach humans.

The experimental nasal spray is being developed by scientists at the University of Helsinki, and it relies on a slightly different approach of combatting the coronavirus than other methods.

“Its prophylactic use is meant to protect from SARS-CoV-2 infection,” study author Kalle Saksela told Gizmodo in an email. “However, it is not a vaccine, nor meant to be an alternative for vaccines, but rather to complement vaccination for providing additional protection for successfully vaccinated individuals in high-risk situations, and especially for immunocompromised persons—for example, those receiving immunosuppressive therapy.”

Vaccines work by training the immune system to recognize a germ without causing disease, which then allows us to produce our own natural supply of antibodies and immune cells specifically tuned to that germ if it appears in the future. We’ve also been able to mass-produce antibodies in the lab to the coronavirus, known as monoclonal antibodies, that can be given to people just after an exposure. The Helsinki team’s treatment, however, is a synthetic protein that’s much smaller than an antibody, but one that can still recognize and bind to the spike protein of the virus. To further amplify the protein’s potential, they smushed together three of them into a single package.

In theory, these antibody-like molecules can proactively inhibit any coronavirus they come into contact with from successfully infecting cells, for a short while at least. The ability to deliver the treatment as a nasal spray also means that these bodyguards can be sent directly into the upper respiratory tract, where most SARS-CoV-2 infections begin. Saksela, a virologist at University of Helsinki, is careful to note that the treatment isn’t intended to replace vaccines or other drugs.

In their research, released as a preprint late last month (meaning it has not been peer reviewed), Saksela and colleagues describe how they tested the spray on pseudoviruses made to look like various variants of the coronavirus, both as they tried to infect cells in a petri dish as well as in live mice.

Omicron has become a major problem largely because its many mutations allow it to partly evade recognition from the natural and lab-made antibodies created against the original strain of the coronavirus. But the team’s molecule apparently targets a region of the coronavirus spike protein that mutates very little. Ideally, this would mean that even Omicron couldn’t easily escape inhibition.

At least in the lab, that’s what Saksela and his team found. Whether it was Omicron, Delta, or the original SARS-CoV-2, the virus was stopped from infecting cells once even a modest dose of the spray was administered. And in mice exposed to the Beta variant of the virus, treated mice were much less likely to have any viral presence throughout their upper respiratory tract and lungs than a control group, with protection being apparent up to eight hours after a dose. The treatment also appeared to be safe and not associated with any noticeable harm.

Of course, this is all basic research that hasn’t yet gone through the full peer-review process. So while the results are definitely encouraging, time will have to tell whether their spray can work the same magic in humans. Should their work continue to show promise, though, Saksela thinks the spray would be valuable even after the pandemic phase of covid-19 has ended.

“This technology is cheap and highly manufacturable, and the inhibitor works equally well against all variants,” he said. “It works also against the now-extinct SARS virus, so it might well also serve as an emergency measure against possible new coronaviruses (SARS-CoV-3 and -4).”

Saksela doesn’t know how long it might take for the spray to reach clinical trials, and from there, to reach the market. He notes the spray could be considered either a drug or medical device, depending on a country’s regulatory process, which would further affect any timeline of development. But aside from continuing to work on a covid-19 treatment, the team might next try to develop a similar spray for other respiratory infections.

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The Coronavirus Can Persist for Months in Brain, Heart, and Intestines: Study

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A positive (L) and a negative antibody test for covid-19 are pictured at a pharmacy in Strasbourg, eastern France, on July 15, 2020.
Photo: Frederick Florin/AFP (Getty Images)

New research this week seems to affirm the suspicion that the coronavirus can infect many parts of the human body, not just our respiratory system. It also found that the virus can sometimes linger in the body even after a person’s initial symptoms have abated. The preliminary findings may shine a light on the complex chronic condition known as long covid that some survivors experience.

SARS-CoV-2 is considered primarily a respiratory virus, much like influenza or other human coronaviruses. In mild cases, its acute symptoms tend to involve the upper respiratory tract, while more serious cases are often associated with lung infection and pneumonia. But evidence from the lab and in patients has suggested that the virus can travel throughout the body and infect other tissues, too, thanks to the receptors it uses to hijack cells. Recently, for instance, scientists found evidence that the coronavirus can readily infect fat and immune cells.

The scientists behind this new research, mostly from the National Institutes of Health, say theirs is the most comprehensive look so far at how well the coronavirus can infect the various parts of the human body and brain. To do this, the researchers performed complete autopsies on 44 people who had been infected with the coronavirus. In all but five cases, the infection was directly implicated in the person’s death.

Overall, the team found copious signs of the coronavirus beyond the respiratory tract, both early and late into the infection. Its presence was definitely highest in the airways and lungs. But they also found evidence of infection in the cardiovascular tissue of nearly 80% of patients; in the gastrointestinal tissue of 73% of patients, and in the muscle, skin, adipose (fat), and peripheral nervous tissue of 68% of patients. Across all 85 body parts and bodily fluids they studied, the virus could be found—at least some of the time—in 79 of them, including the brain. And they found traces of viral RNA throughout the body and brain months after symptoms had begun, up to 230 days in one patient’s case.

“Our data prove that SARS-CoV-2 causes systemic infection and can persist in the body for months,” the authors wrote in their paper, which was released as a preprint Sunday but is under review for publication in the journal Nature, according to Bloomberg News.

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There are important limitations to this research. For one, the cases obviously tended to involve people severely ill with covid-19. But even in the few cases where someone had mild or no covid-related symptoms, the virus could still be found throughout the body, the authors noted. The study was also conducted between April 2020 to March 2021, a period of time when relatively few people were vaccinated. So it’s possible that those with some immunity may prevent the virus from infecting the body as thoroughly as it did in these patients (there was no mention of anyone being vaccinated in the paper). The emergence of several new variants of the virus, such as Delta and Omicron, since March may further complicate the picture.

All that said, the findings give us a clearer picture of how acute infection by SARS-CoV-2 works and how it could continue to cause trouble after the initial illness seems to resolve. Some experts believe that at least some cases of long covid can be attributed to persistent infection. But while these findings provide strong evidence that long-term infections do happen, they also raise new questions.

For instance, the team found little evidence that the presence of the virus outside the lungs was associated with direct inflammation or other virus-related injury to cells, even in persistent infections. That’s key because inflammation is one of the most common ways that the body can damage itself chronically, and many experts believe that it plays a major role in long covid symptoms. In some cases of persistent infection, the authors noted, the virus may have been too defective to keep replicating, which may explain why the body didn’t respond to it like a typical infection. This finding doesn’t exclude the possibility that the virus is still causing harm when it lingers in the body, but it adds a new wrinkle to the mystery of long covid that scientists will have to keep studying.

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CDC’s New, Shorter Covid-19 Isolation Guidelines Disturb Some Health Experts

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People at a testing site located in the international terminal at Los Angeles International Airport (LAX) on December 21, 2021
Photo: Mario Tama (Getty Images)

Fresh off the Christmas holiday, the Centers for Disease Control and Prevention has updated its guidance on how long people should isolate away from others if they’ve been infected by or exposed to the coronavirus. The change effectively cuts the waiting period in half for many people, particularly those without symptoms. But at least some experts aren’t too pleased, arguing that the new recommendations are too lenient, since they largely won’t depend on testing, and that people’s health is being placed in danger to placate business interests.

The CDC announced the changes on Monday afternoon. Previously, people who tested positive for covid-19 have been told to isolate at home for 10 days, starting from their positive test result. Now, the CDC says that people should isolate for five days, then, if they have no symptoms, they can interact with others but should wear a mask for the remaining five days.

For those who suspect they’ve been recently exposed, the CDC now recommends that people who are unvaccinated or who had received their primary vaccine series more than six months ago should quarantine for five days, then wear a mask for the remaining five days (ideally getting tested for covid-19 around day five). If they’re unable to quarantine, then they should wear a mask all 10 days. Lastly, for those exposed who have gotten all their shots, including a booster, they’re recommended to wear a mask for 10 days but don’t have to quarantine/isolate if they’re not experiencing symptoms.

There have been numerous studies suggesting that people are most infectious right before they get sick and for a few days afterward. Other research has shown that this window of infection may close even sooner for vaccinated people who develop a breakthrough infection. And in justifying the new guidance, the CDC did reference this data. “The change is motivated by science demonstrating that the majority of SARS-CoV-2 transmission occurs early in the course of illness, generally in the 1-2 days prior to onset of symptoms and the 2-3 days after,” the CDC wrote in its explanation of the changes Monday.

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Yet, the evidence isn’t as cut-and-dry as the CDC makes it appear, according to Justin Feldman, a social epidemiologist at Harvard who has studied the disparate impacts of the pandemic within the U.S.

“The CDC’s move to shorten isolation to 5 days, with no requirement to test negative before going back to work, is reckless and dangerous,” Feldman told Gizmodo. “There is a lot of variability in how long people stay contagious, and many can still infect others after 5 days.”

Ellie Murray, an epidemiology professor at ​​the Boston University School of Public Health, notes that the data cited by the CDC to warrant this change isn’t particularly ground-breaking. “Shortening the isolation period does not seem to be based on any new data about the virus or how it spreads, and epidemiologically there’s no new evidence to support this change. I do not think that it will help if the goal is to keep cases as low as possible,” she told Gizmodo.

Indeed, while some experts are generally supportive of the isolation period being made shorter, they’ve still been critical about the lack of advice for people to get tested before leaving isolation. The UK recently shortened its recommendations for isolation from 10 days to seven days for most people, but only if the person tests negative on two rapid lateral flow tests two days in a row. Strangely enough, the CDC did follow in the UK’s footsteps, but only for healthcare workers. As of last week, healthcare workers are now recommended to return to work after seven days, if they test negative and are asymptomatic; however, “isolation time can be cut further if there are staffing shortages.”

“It makes a great deal of sense to allow some people to leave isolation in fewer than 10 days,” Carl Bergstrom, a professor of biology at the University of Washington, told Gizmodo. “The devil is in the details though. How much fewer, and what precisely should be the criteria? The CDC press release doesn’t answer this.”

Adding to the confusion is that the five-day rule is ostensibly meant for people who are asymptomatic—in other words, not feeling sick at all. Yet on the same page explaining the change, the CDC later says that this also applies to people whose symptoms are “resolving” after five days. Those with fever, however, are still being told to isolate longer.

“For previous strains, the infectious period was considerably longer than five days in many though not all patients. Does the CDC believe that this is changed?” Bergstrom said. “Is the thought that vaccination or prior infection status reduces the infectious interval—and if so, should that be accounted for in the recommendation? Is this some kind of cost-benefit calculation? We aren’t given enough information to know.”

The elephant in the room is that these changes do not appear to be solely motivated by the science surrounding covid-19 transmission. Just a week ago, Delta Air Lines CEO Ed Bastian publicly pleaded with the CDC to cut the recommended isolation period for fully vaccinated people with breakthrough infections, citing the impacts it was having on his workforce. And many experts, along with workers’ unions, do believe that this is more about getting people to work than keeping others safe from covid-19.

“It is a clear case of prioritizing corporate profit over public health, and it’s happening at a time when many hospitals are starting to become overwhelmed with covid-19 patients,” Feldman said.

The country is in the midst of a resurgent wave of the pandemic, with case loads rising in some areas to the highest levels seen yet, fueled by the emergence of the Omicron variant. And while Omicron does appear to be milder than the recently dominant Delta variant, it may not be any less of a problem than past strains of the coronavirus. Much like previous waves, it’s not just cases but hospitalizations and deaths that now appear to be on the rise.

It’s possible that this change may not affect the trajectory of the pandemic much, since people are generally less infectious after a few days. But it’s perhaps another example of the CDC losing the trust of the public in recent months (on social media, scientists and others are now parodying the CDC’s business-friendly advice). The new recommendations may also just be counterproductive, according to Murray, if you’re hoping to get everyone back to work as soon as possible.

“It seems very short-sighted to imagine that workplace absences are not going to be coupled to case levels. Workplaces being full of infectious employees will just mean more and more staffing issues,” she noted. “Accepting some closures now to get this surge under control would result in fewer staffing issues in January—if that’s really all they care about—and less covid.”



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Uh Oh, the Coronavirus Has Been Spreading Widely in U.S. Deer

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White-tailed deer in Delaware
Photo: Eva HAMBACH / AFP (Getty Images)

The coronavirus behind covid-19 appears to have found another species in which it can easily reproduce and spread. Preliminary research out this week seems to confirm that the virus is now freely circulating among wild deer. Though it’s unclear how important this discovery may be, it’s possible that it could affect our own future with covid-19.

Coronaviruses in general are known for their ability to infect a wide range of species—a trait that made them prime suspects for causing a pandemic, even before covid-19 arrived. And while the true origins of this pandemic are still being argued over, it’s clear that it didn’t take long for SARS-CoV-2 to make itself comfortable in other animals beside us. Cats, dogs, weasels, and even other primates like gorillas have all been documented carriers of the virus, along with deer.

In most of these reported animal outbreaks, humans have been implicated as the initial source of transmission. The virus has also been shown to be capable of spreading from animal to animal, particularly among weasels. These have often been isolated incidents, such as zoos where a worker might infect a few animals before the chain of transmission stops there. This new research, released as a preprint paper on Biorxiv, suggests that the virus has truly spilled over into at least some populations of white-tailed deer in the U.S. and is now widely spreading among them.

Researchers at Penn State and elsewhere tested lymph node samples collected from nearly 300 captive and free-living deer living in Iowa, looking for the presence of coronavirus RNA. The samples came from an already-established surveillance program for chronic wasting disease, an emerging illness in deer that many states are tracking. Between September 2020 and January 2021, about a third of these samples tested positive for the virus.

What’s more, the samples from free-living deer were more likely to test positive for the virus than captive populations (including those living on preserves). And when the authors tried to map out the geographic distribution and genetic signature of these cases, they determined that the virus had jumped over from humans to deer multiple times during those months and that it was then spreading among free-living deer.

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In August, scientists with the USDA released research suggesting that up to 40% of deer in Michigan, New York, Illinois, and Pennsylvania carried antibodies to the coronavirus. But the authors say theirs is the first to show that the virus is almost certainly circulating among wild white-tailed deer, the most abundant deer species in North America. And that could carry some serious ramifications for our journey with the coronavirus moving forward.

“Our results suggest that deer have the potential to emerge as a major reservoir host for SARS-CoV-2, a finding that has important implications for the virus genomic diversity and future trajectory of the pandemic,” the authors wrote.

As they explain in the paper, viruses that only have one major host are easier to track and predict on an evolutionary level. But a virus that jumps between multiple species can pick up a wider array of mutations as it adapts, some of which could make the virus more likely to evade a person’s existing immunity or more likely to cause serious illness. A more traveled SARS-CoV-2 also has opportunity to mingle with other coronavirus species, allowing for unlucky genetic jumbles to occur. We see this dynamic play out already with influenza, which mutates very quickly for a virus but also occasionally swaps genes with the influenza viruses common to birds and pigs. Sometimes, this mix can produce a pandemic strain of flu on top of the seasonal flu we deal with every year. The coronavirus could also mutate to become more dangerous to deer, though lab experiments have suggested that most infected deer do not become sick currently.

If nothing else, simply having another place to crash could allow the coronavirus to bide its time before coming back into our lives. As the researchers note, “animal reservoirs can provide a refuge outside of a largely immune/vaccinated human population and thus represents a looming threat of reemergence into humans.”

Of course, the pandemic is still in our present. Much of the world remains unvaccinated, and it may take years before the virus will run out of fresh human bodies to easily infect. And it’s not inevitable that a deervid-19 would return with a vengeance down the line to severely plague humanity again. The virus may not actually become endemic in deer as it will in humans, but the potential risks posed by another nearby animal host of the coronavirus are definitely worth keeping an eye on, the authors say.

“Given the social and economic importance of deer to the U.S. economy, even while experimental evidence suggest that SARS-CoV-2 infected deer remain largely asymptomatic, the clinical outcomes and health implications of SARS-CoV-2 infection in free-living deer are unknown and warrant further investigation,” they wrote.

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Doctors Say Mild Covid-19 Likely Triggered Psychiatric Illness in Two Teen Patients

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A MRI scan of one of the patients, with the arrow pointing to a suspected lesion.
Photo: Bartley CM, et al/JAMA Neurology

Researchers in California suspect that covid-19 triggered sudden mental illness in at least two of their teenage patients. Though they caution that a causative link remains uncertain, they say they’ve found evidence of antibodies attacking the brain of their patients post-infection, which could help explain the psychiatric symptoms.

Since the very start of the pandemic, some researchers have warned that covid-19 could contribute to a wave of neurological illness, based on the history of previous pandemics. Since then, studies have shown that covid-19 survivors do seem to be at higher risk for ailments like depression and anxiety. Some researchers and patient advocates have also argued that long covid—the constellation of chronic symptoms reported by some survivors—can include neurological impairments.

The stress of simply having covid-19 could certainly influence a person’s mental health, as could the aftereffects of a severe infection and hospitalization. But it’s possible that the virus itself could directly impact the nervous system and brain, even in mild cases, and these interactions could then lead to a higher risk of neurological and psychiatric disorders. Because mental illness is unfortunately common and often linked to a variety of influences, it can be difficult to show cause and effect from any one thing, including a viral infection.

But doctors at the University of California, San Francisco (UCSF) Benioff Children’s Hospital say they’ve come across a few cases in the past year where covid-19 does seem to have been a primary trigger for a patient’s sudden mental illness. In a new paper published Monday in JAMA Neurology, they describe teen patients who developed newly documented psychiatric symptoms, including extreme mood swings, paranoid delusions, and suicidal ideation, after a confirmed but mild or asymptomatic case of covid-19. It’s the timing of these events that suggests the symptoms were connected to the infection, study author Sam Pleasure, a UCSF neurologist, told Gizmodo.

In the spinal fluid of two patients, the team also found antibodies to the coronavirus, known as SARS-COV-2, as well as autoantibodies to the nervous system. In one patient, these traitor antibodies seemed to target a gene responsible for making a protein called transcription factor 4 (TCF4), which is notable because variations of the gene have been linked to psychiatric disorders including schizophrenia. The patients had a history of some mental health problems, such as anxiety and tics, but not to the extent documented by the doctors.

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A third teenage patient had neither kind of antibody in their nervous system, and it was determined that the most likely cause of their symptoms was an unknown drug they had taken days earlier.

But with the other two, those antibodies indicate that the coronavirus can reach the nervous system and stir up trouble there. It may be that the virus isn’t directly causing these symptoms, but rather that it helps generate a self-destructive immune response.

“We know that covid-19 is a potent stimulus for increased inflammatory responses, and one possible cause of these symptoms is that they are associated with this ‘generic’ increase in inflammation,” Pleasure explained in an email.

In the two patients where covid-19 was seen as a likely trigger, the doctors chose to treat them with immunotherapy, including steroids to tamp down inflammation. One patient seemed to respond well and by a month later had stopped reporting delusions and twitching. The second patient seemed to respond modestly to the immunotherapy, and by the six-month mark they were still improved but continued to have memory problems and trouble concentrating.

The authors found other reports of similarly timed cases among hospitalized adult covid-19 patients. Pleasure noted that immune-related problems after an infection have been documented well before covid-19, often linked to viral infections. These post-infection cases in general seem to be rare, but there are still many unknowns.

“We don’t at this point know how common this is with covid-19 infection and may be seeing patients primarily because of the very large numbers of infected people at about the same time,” Pleasure said.

To better understand these cases and definitively establish a link between sudden psychiatric illness and covid-19 would require more research, which the authors say they’re conducting now.

“We are working on studying larger numbers of prospectively followed patients with post-covid neurologic and psychiatric symptoms,” Pleasure said. “We are also able to compare such patients to ‘controls,’ i.e. patients after covid without neuropsychiatric symptoms.”

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