Tag Archives: infect

Scientists fear 100% fatal ‘zombie deer disease’ is evolving to infect humans in forests across America – Daily Mail

  1. Scientists fear 100% fatal ‘zombie deer disease’ is evolving to infect humans in forests across America Daily Mail
  2. Zombie deer disease is spreading and scientists are concerned that it could jump to humans The Conversation
  3. Scientists increasingly worried that chronic wasting disease could jump from deer to humans Star Tribune
  4. Devastating deer disease found in six more Mississippi counties, including on the MS Coast Biloxi Sun Herald
  5. Louisiana detected seven new CWD positives since July – Mississippi’s Best Community Newspaper | Mississippi’s Best Community Newspaper Natchez Democrat

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SARS-CoV-2 virus found to migrate within neurons and infect the brain – Medical Xpress

  1. SARS-CoV-2 virus found to migrate within neurons and infect the brain Medical Xpress
  2. Effectiveness of the second COVID-19 booster against Omicron: a large-scale cohort study in Chile Nature.com
  3. Early Detection and Surveillance of the SARS-CoV-2 … CDC
  4. JN.1: The Odd Man Out Among Omicron Sublineages (Updated) Forbes
  5. Assessment of hybrid population immunity to SARS-CoV-2 following breakthrough infections of distinct SARS-CoV-2 variants by the detection of antibodies to nucleoprotein | Scientific Reports Nature.com
  6. View Full Coverage on Google News

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COVID-19 was engineered as ‘bioweapon’ to purposely infect people, claims Wuhan researcher – WION

  1. COVID-19 was engineered as ‘bioweapon’ to purposely infect people, claims Wuhan researcher WION
  2. Covid 19 | Did China Use Covid 19 As A Biological Weapon? Jennifer Zeng Exclusive Interview CNN-News18
  3. Intentional Bioweapon? Wuhan Researcher Makes Shocking Claims on COVID Origin | Weather.com The Weather Channel
  4. Wuhan researcher claims China engineered COVID-19 as a bioweapon to infect people | WION LIVE WION
  5. China engineered Covid-19 bioweapon to purposely infect people, reveals Wuhan researcher Firstpost
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What Is Spillover? How Animal Viruses Infect Humans | Weather.com – The Weather Channel

  1. What Is Spillover? How Animal Viruses Infect Humans | Weather.com The Weather Channel
  2. Bird flu: Nigeria is on major migratory bird routes, new strains keep appearing theconversation.com
  3. Highly Pathogenic Avian Influenza Is Devastating Birds, and Humans May Be Next The Daily Beast
  4. How to Handle the Bird Flu: America Must Prepare for the Next Possible Pandemic Foreign Affairs Magazine
  5. As bird flu continues to spread in the US and worldwide, what’s the risk that it could start a human pandemic? 4 questions answered theconversation.com
  6. View Full Coverage on Google News

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All You Need To Know About Russian Bat Virus That Could Infect Humans

All you need to know about Khosta-2

US scientists have discovered a new virus in bats that could be bad news for humans. The new virus, called Khosta-2 cannot just infect human cells, it is also resistant to current vaccines. Research published in the journal PLOS Pathogens says that the virus is resistant to the antibodies of people vaccinated against SARS-CoV-2—which causes COVID-19, reported Newsweek.

The virus was first discovered in bats in Russia in 2020 but at that time scientists did not think that the virus posed a threat to humans. After much careful research done by scientists, they found that the virus can infect human cells and it can become a possible public health threat.

What is Khosta-2?

Sarbecovirus, to which Khosta-2 and SARS-CoV-2 belong, is a subgroup of coronaviruses.

According to a report in Time magazine, a related virus also found in the Russian bats, Khosta-1, could not enter human cells readily, but Khosta-2 could. Khosta-2 attaches to the same protein, ACE2 that SARS-CoV-2 uses to penetrate human cells. A researcher says that receptors on human cells are the way that viruses get into cells. If a virus can’t get in the door, then it can’t get into the cell, and it’s difficult to establish any type of infection. The new virus can impact human cells readily. Michael Letko, an author of the study says that people vaccinated against covid-19 cannot neutralize the virus, and neither can people who have recovered from Omicron infections.

However, the researchers say that like the Omicron variant of SARS-CoV-2, this virus does not have genes that can cause serious disease in people. But it can eventually change if it gets mixed with genes of SARS-CoV-2.

How does it spread?

Khosta-2 has been circulating in wildlife such as bats, pangolins, raccoon dogs and palm civets. Mr Letko told Newsweek, it is difficult to say at this stage whether Khosta-2 has the potential to spark an epidemic or even a pandemic.

The scientists warn that if Khosta-2 combines with SARS-CoV-2, it can have more infectious factors. “The chances of SARS-CoV-2 ever ‘meeting’ Khosta-2 in nature is surely very small, but there have been an increasing number of reports describing SARS-CoV-2 spilling back into wildlife—like white-tailed deer on the East Coast of the United States,” Letko said.

Vaccine research

“Right now, there are groups trying to come up with a vaccine that doesn’t just protect against the next variant of SARS-2 (SARS-CoV-2) but actually protects us against the sarbecoviruses in general,” Letko said.

He added, “Unfortunately, many of our current vaccines are designed [for] specific viruses we know infect human cells or those that seem to pose the biggest risk to infect us. But that’s a list that’s ever-changing. We need to broaden the design of these vaccines to protect against all sarbecoviruses,” added Letko.

Known cases across the world

The virus lacks some of the genes believed to be involved in pathogenesis — that is, developing into a disease — in humans.

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Khosta-2: New Russian bat virus discovered that could infect humans and resist COVID vaccines

When SARS-CoV-2 – the virus behind COVID-19 – surfaced in China and quickly brought the entire world to a standstill, then-President Donald Trump liked to refer to it as “the Chinese virus”.

Fast forward two and a half years, and US scientists are warning that a newly-discovered virus harboured by Russian horseshoe bats is also capable of infecting humans and evading COVID-19 antibodies and vaccines.

The bat virus, named Khosta-2, is known as a sarbecovirus – the same sub-category of coronaviruses as SARS-CoV-2 – and it displays “troubling traits,” according to a new study published in the journal PLoS Pathogens.

A team led by researchers at the Paul G. Allen School for Global Health at Washington State University (WSU) found that Khosta-2 can use its spike proteins to infect human cells very much like SARS-CoV-2 does.

“Our research further demonstrates that sarbecoviruses circulating in wildlife outside of Asia – even in places like western Russia where the Khosta-2 virus was found – also pose a threat to global health and ongoing vaccine campaigns against SARS-CoV-2,” Michael Letko, a virologist at WSU and corresponding author of the study, said in a statement.

He said this discovery highlights the need to develop new vaccines that don’t only target known variants of SARS-CoV-2, such as Omicron, but that protect against all sarbecoviruses.

‘Weird Russian viruses’

Among the hundreds of sarbecoviruses discovered in recent years, most have been found in Asian bats and are not capable of infecting human cells.

The Khosta-1 and Khosta-2 viruses were discovered in bats near Russia’s Sochi National Park in 2020, and it initially appeared they were not a threat to humans, according to the study’s authors.

“Genetically, these weird Russian viruses looked like some of the others that had been discovered elsewhere around the world, but because they did not look like SARS-CoV-2, no one thought they were really anything to get too excited about,” Letko said.

“But when we looked at them more, we were really surprised to find they could infect human cells. That changes a little bit of our understanding of these viruses, where they come from and what regions are concerning”.

‘Troubling traits’

Letko and his colleagues determined that Khosta-1 posed a low risk to humans, but Khosta-2 was more concerning.

In particular, like SARS-CoV-2, Khosta-2 can use its spike protein to infect cells by attaching to a receptor protein, called angiotensin-converting enzyme 2 (ACE2), which is found throughout human cells.

The scientists next wanted to find out whether the virus could evade the immunity offered either by previous coronavirus infections or COVID-19 vaccines.

Using serum derived from people vaccinated against COVID-19, the team discovered Khosta-2 was not neutralised by current vaccines.

They also tested serum from people who were infected with the Omicron variant, but there again, the antibodies were ineffective.

Fortunately, the authors write that the new virus lacks some of the genetic features thought to “antagonise” the immune system and contribute to disease in humans – but there is a risk that Khosta-2 could wreak havoc by recombining with a second virus such as SARS-CoV-2.

“When you see SARS-2 has this ability to spill back from humans and into wildlife, and then there are other viruses like Khosta-2 waiting in those animals with these properties we really don’t want them to have, it sets up this scenario where you keep rolling the dice until they combine to make a potentially riskier virus,” Letko said.

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Monkeypox could infect children by the end of the year

Monkeypox cases could spiral by the end of the year – and reach children, for whom the virus can be deadly – if efforts to vaccinate against it are not improved, experts have warned.

While 50,000 vaccine doses are on order, public health experts say four times this number will be needed to halt the spread.

In the UK, there have already been more than 1,850 cases of the disease, which causes painful blisters across the body, and numbers are believed to be doubling every 15 days. These have predominantly been seen in gay men.

Dr Deborah Birx, the former head of the US Covid task force, told The Mail on Sunday that all gay men in London under the age of 50 should be vaccinated as well as women who visit gay bars. ‘If you’re at a gay bar and you’re dancing, then there is a risk of infection,’ she said.

Monkeypox cases could spiral by the end of the year – and reach children, for whom the virus can be deadly – if efforts to vaccinate against it are not improved, experts have warned

The virus is passed on through close physical contact, such as sex, but also kissing and hugging.

Vaccines can provide effective protection, but doctors have criticised the slow rollout of the jabs to Britons most at risk and claim the UK does not have not enough doses to stop the virus from spreading into the wider population.

There are particular worries that monkeypox could reach children, who are more likely to suffer severe illness as a result.

On Thursday, the UK Health Security Agency confirmed that a London school sent reception classes home until the end of term after a child came into contact with a monkeypox case.

According to a letter sent to parents, officials advised parents to avoid hugging their children, or any other very close contact, for two weeks. The children will now be offered the vaccine.

Dr Deborah Birx (pictured), the former head of the US Covid task force, told The Mail on Sunday that all gay men in London under the age of 50 should be vaccinated as well as women who visit gay bars. ‘If you’re at a gay bar and you’re dancing, then there is a risk of infection,’ she said

There are two vaccines that can protect against the virus. One, created by a small Danish company, specifically protects against monkeypox. But the decades-old smallpox vaccine also works, because the two viruses are so similar.

The majority of over-50s are thought already to have good immunity to monkeypox because they would have received a compulsory smallpox jab in the 1970s and 1980s.

The Mail on Sunday understands the UK has 30,000 vaccines – a combination of the two types – and sexual health clinics last week began inviting some gay men to receive the jab.

However, experts say at least 200,000 doses of the jab are needed to prevent monkeypox spreading and reaching children, and spreading among them and other vulnerable groups such as pregnant women. 

This figure is based on the number of men eligible for HIV-preventative drugs – those who have on average two or more male partners every six months, and as such are at most risk of catching monkeypox.

If health officials are able to vaccinate this group, experts believe the disease could be effectively controlled.

Examples of the monkeypox rash, which can appear anywhere on the body. In the UK, there have already been more than 1,850 cases of the disease, which causes painful blisters, and numbers are believed to be doubling every 15 days. These have predominantly been seen in gay men

Official estimates suggest there are 100,000 men eligible for these drugs in the UK, 70,000 of whom are in London, where the majority of monkeypox cases have already been seen.

As with Covid, two jabs are required for the vaccine to have full effect, meaning that, at present, the UK cannot vaccinate all eligible Britons.

‘Health officials have told us the current strategy is to get hold of 50,000 doses of the vaccine, but since we need to give out two doses, that means only 25,000 people will get them and that’s not nearly enough,’ says Dr Claire Dewsnap, president of the British Association for Sexual Health and HIV. 

‘Currently monkeypox is just affecting this sub-group of Britons, but if cases keep rising it won’t stay that way. When it eventually breaks out into the wider population, we’ll need a lot more vaccines than we can feasibly get our hands on.’

Experts also believe there are many cases going undiagnosed, following a study last week from the Institute of Tropical Medicine in Belgium, which showed transmission of the virus may occur without symptoms.

More than ten per cent of Britons infected have been hospitalised, though this has predominantly been for pain management, as the blisters can be debilitating, making activities such as eating and going to the toilet excruciating. In people with weaker immune systems, like children, the disease can be deadly.

In June, World Health Organisation director-general Tedros Adhanom Ghebreyesus said he was concerned that sustained transmission of monkeypox would lead to the virus establishing itself in the community and could infect ‘high-risk groups including children, the immunocompromised and pregnant women’.

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Which Animal Viruses Could Infect People? Computers Are Racing to Find Out.

Colin Carlson, a biologist at Georgetown University, has started to worry about mousepox.

The virus, discovered in 1930, spreads among mice, killing them with ruthless efficiency. But scientists have never considered it a potential threat to humans. Now Dr. Carlson, his colleagues and their computers aren’t so sure.

Using a technique known as machine learning, the researchers have spent the past few years programming computers to teach themselves about viruses that can infect human cells. The computers have combed through vast amounts of information about the biology and ecology of the animal hosts of those viruses, as well as the genomes and other features of the viruses themselves. Over time, the computers came to recognize certain factors that would predict whether a virus has the potential to spill over into humans.

Once the computers proved their mettle on viruses that scientists had already studied intensely, Dr. Carlson and his colleagues deployed them on the unknown, ultimately producing a short list of animal viruses with the potential to jump the species barrier and cause human outbreaks.

In the latest runs, the algorithms unexpectedly put the mousepox virus in the top ranks of risky pathogens.

“Every time we run this model, it comes up super high,” Dr. Carlson said.

Puzzled, Dr. Carlson and his colleagues rooted around in the scientific literature. They came across documentation of a long-forgotten outbreak in 1987 in rural China. Schoolchildren came down with an infection that caused sore throats and inflammation in their hands and feet.

Years later, a team of scientists ran tests on throat swabs that had been collected during the outbreak and put into storage. These samples, as the group reported in 2012, contained mousepox DNA. But their study garnered little notice, and a decade later mousepox is still not considered a threat to humans.

If the computer programmed by Dr. Carlson and his colleagues is right, the virus deserves a new look.

“It’s just crazy that this was lost in the vast pile of stuff that public health has to sift through,” he said. “This actually changes the way that we think about this virus.”

Scientists have identified about 250 human diseases that arose when an animal virus jumped the species barrier. H.I.V. jumped from chimpanzees, for example, and the new coronavirus originated in bats.

Ideally, scientists would like to recognize the next spillover virus before it has started infecting people. But there are far too many animal viruses for virologists to study. Scientists have identified more than 1,000 viruses in mammals, but that is most likely a tiny fraction of the true number. Some researchers suspect mammals carry tens of thousands of viruses, while others put the number in the hundreds of thousands.

To identify potential new spillovers, researchers like Dr. Carlson are using computers to spot hidden patterns in scientific data. The machines can zero in on viruses that may be particularly likely to give rise to a human disease, for example, and can also predict which animals are most likely to harbor dangerous viruses we don’t yet know about.

“It feels like you have a new set of eyes,” said Barbara Han, a disease ecologist at the Cary Institute of Ecosystem Studies in Millbrook, N.Y., who collaborates with Dr. Carlson. “You just can’t see in as many dimensions as the model can.”

Dr. Han first came across machine learning in 2010. Computer scientists had been developing the technique for decades, and were starting to build powerful tools with it. These days, machine learning enables computers to spot fraudulent credit charges and recognize people’s faces.

But few researchers had applied machine learning to diseases. Dr. Han wondered if she could use it to answer open questions, such as why less than 10 percent of rodent species harbor pathogens known to infect humans.

She fed a computer information about various rodent species from an online database — everything from their age at weaning to their population density. The computer then looked for features of the rodents known to harbor high numbers of species-jumping pathogens.

Once the computer created a model, she tested it against another group of rodent species, seeing how well it could guess which ones were laden with disease-causing agents. Eventually, the computer’s model reached an accuracy of 90 percent.

Then Dr. Han turned to rodents that have yet to be examined for spillover pathogens and put together a list of high-priority species. Dr. Han and her colleagues predicted that species such as the montane vole and Northern grasshopper mouse of western North America would be particularly likely to carry worrisome pathogens.

Of all the traits Dr. Han and her colleagues provided to their computer, the one that mattered most was the life span of the rodents. Species that die young turn out to carry more pathogens, perhaps because evolution put more of their resources into reproducing than in building a strong immune system.

These results involved years of painstaking research in which Dr. Han and her colleagues combed through ecological databases and scientific studies looking for useful data. More recently, researchers have sped this work up by building databases expressly designed to teach computers about viruses and their hosts.

In March, for example, Dr. Carlson and his colleagues unveiled an open-access database called VIRION, which has amassed half a million pieces of information about 9,521 viruses and their 3,692 animal hosts — and is still growing.

Databases like VIRION are now making it possible to ask more focused questions about new pandemics. When the Covid pandemic struck, it soon became clear that it was caused by a new virus called SARS-CoV-2. Dr. Carlson, Dr. Han and their colleagues created programs to identify the animals most likely to harbor relatives of the new coronavirus.

SARS-CoV-2 belongs to a group of species called betacoronaviruses, which also includes the viruses that caused the SARS and MERS epidemics among humans. For the most part, betacoronaviruses infect bats. When SARS-CoV-2 was discovered in January 2020, 79 species of bats were known to carry them.

But scientists have not systematically searched all 1,447 species of bats for betacoronaviruses, and such a project would take many years to complete.

By feeding biological data about the various types of bats — their diet, the length of their wings, and so on — into their computer, Dr. Carlson, Dr. Han and their colleagues created a model that could offer predictions about the bats most likely to harbor betacoronaviruses. They found over 300 species that fit the bill.

Since that prediction in 2020, researchers have indeed found betacoronaviruses in 47 species of bats — all of which were on the prediction lists produced by some of the computer models they had created for their study.

Daniel Becker, a disease ecologist at the University of Oklahoma who also worked on the betacoronavirus study, said it was striking the way simple features such as body size could lead to powerful predictions about viruses. “A lot of it is the low-hanging fruit of comparative biology,” he said.

Dr. Becker is now following up from his own backyard on the list of potential betacoronavirus hosts. It turns out that some bats in Oklahoma are predicted to harbor them.

If Dr. Becker does find a backyard betacoronavirus, he won’t be in a position to say immediately that it is an imminent threat to humans. Scientists would first have to carry out painstaking experiments to judge the risk.

Pranav Pandit, an epidemiologist at the University of California at Davis, cautions that these models are very much a work in progress. When tested on well-studied viruses, they do substantially better than random chance, but could do better.

“It’s not at a stage where we can just take those results and create an alert to start telling the world, ‘This is a zoonotic virus,’” he said.

Nardus Mollentze, a computational virologist at the University of Glasgow, and his colleagues have pioneered a method that could markedly increase the accuracy of the models. Rather than looking at a virus’s hosts, their models look at its genes. A computer can be taught to recognize subtle features in the genes of viruses that can infect humans.

In their first report on this technique, Dr. Mollentze and his colleagues developed a model that could correctly recognize human-infecting viruses more than 70 percent of the time. Dr. Mollentze can’t yet say why his gene-based model worked, but he has some ideas. Our cells can recognize foreign genes and send out an alarm to the immune system. Viruses that can infect our cells may have the ability to mimic our own DNA as a kind of viral camouflage.

When they applied the model to animal viruses, they came up with a list of 272 species at high risk of spilling over. That’s too many for virologists to study in any depth.

“You can only work on so many viruses,” said Emmie de Wit, a virologist at Rocky Mountain Laboratories in Hamilton, Mont., who oversees research on the new coronavirus, influenza and other viruses. “On our end, we would really need to narrow it down.”

Dr. Mollentze acknowledged that he and his colleagues need to find a way to pinpoint the worst of the worst among animal viruses. “This is only a start,” he said.

To follow up on his initial study, Dr. Mollentze is working with Dr. Carlson and his colleagues to merge data about the genes of viruses with data related to the biology and ecology of their hosts. The researchers are getting some promising results from this approach, including the tantalizing mousepox lead.

Other kinds of data may make the predictions even better. One of the most important features of a virus, for example, is the coating of sugar molecules on its surface. Different viruses end up with different patterns of sugar molecules, and that arrangement can have a huge impact on their success. Some viruses can use this molecular frosting to hide from their host’s immune system. In other cases, the virus can use its sugar molecules to latch on to new cells, triggering a new infection.

This month, Dr. Carlson and his colleagues posted a commentary online asserting that machine learning may gain a lot of insights from the sugar coating of viruses and their hosts. Scientists have already gathered a lot of that knowledge, but it has yet to be put into a form that computers can learn from.

“My gut sense is that we know a lot more than we think,” Dr. Carlson said.

Dr. de Wit said that machine learning models could some day guide virologists like herself to study certain animal viruses. “There’s definitely a great benefit that’s going to come from this,” she said.

But she noted that the models so far have focused mainly on a pathogen’s potential for infecting human cells. Before causing a new human disease, a virus also has to spread from one person to another and cause serious symptoms along the way. She’s waiting for a new generation of machine learning models that can make those predictions, too.

“What we really want to know is not necessarily which viruses can infect humans, but which viruses can cause an outbreak,” she said. “So that’s really the next step that we need to figure out.”

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COVID-19 can infect penis and testicle cells

Covid can may be able to infect and damage a person’s penis and testicles, a new study finds.

Researchers from Northwestern University Feinberg School of Medicine, in Chicago, Illinois, found in a study of monkeys that the virus could infect the cells of male genitalia, and cause long-term harm.

Researchers found that COVID-19 infecting a person’s penis, testicle and prostate cells can cause a variety of health issues

Previous research has found that male survivors of the virus sometimes suffer erectile dysfunction and other genital tract issues, though it is often believed to be  a result of inflammation as an immune response to the virus.

These researchers now believe that it is the virus itself, not the immune system, causing genital issues for infected males, changing the calculous for how this type of condition would be treated.

Researchers, who posted their findings last week in bioRxiv pending peer review before journal publication, performed research on three male rhesus macaques, a breed of monkey often used for such studies because they have many genetic similarities with humans.  

Each of the monkeys had body scans performed on them after they were infected with the virus in an effort to detect where traces of the virus were visible.

Dr Thomas Hope, lead researcher and a biology professor at Northwestern, told the New York Times that ‘the signal in the penis was off the radar.’

Researchers found spread of the virus in the penis of all three animals. One of the animals had infection in its testicles as well. 

The findings indicate that the virus managed to infect and spread within the monkey’s penis, likely causing the animals genital tract issues, like erectile dysfunction.

The study was performed on male rhesus macaques (pictured), a type of monkey that has many genetic similarities to humans

Researchers believe this type of spread can cause major damage to the region of the body in both animals and humans.

Virus spread in the penis can cause erectile dysfunction and peyronie’s disease, a condition where a person feels intense pain when they get an erection.

Covid spread in the prostate can lead to decreased semen quality and even put a person at a higher risk of developing prostate cancer.

In the testicles, the virus can decreases the count and quality of sperm and reduce testosterones levels.

An infected male may also feel inflammation or pain in their testicles. 

Previous research has found a link between COVID-19 infection and the development of erectile dysfunction.

A study published last year by the University of Florida found that men who had recovered from the virus are three times more likely to develop the condition than those that had not.

Men with pre-existing risk factors like obesity, or a heart or respiratory condition showed an even higher rate of erectile dysfunction.

May have attributed this to inflammation as an immune response to the virus, which is the cause of many ‘long Covid’ symptoms – often placed under the umbrella of MIS-C.

In this case, though, the virus itself is binding itself to the body and causing long-term harm to those that it infects.

‘The receptor that the coronavirus binds to is abundant on the penis and testes,’ Dr Joseph Katz, a dentistry professor at the University of Florida that led last year’s study, said. 

‘The virus can bind to those areas. And research has shown that COVID can reduce the amount of testosterone produced. The loss of testosterone has been shown to put someone at risk of having a more severe outcome from COVID-19.’ 

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COVID loses 50% of ability to infect after 10 seconds in office air: study

The coronavirus loses about 50 percent of its ability to infect about 10 seconds after it becomes airborne in a typical office environment, according to a new study about how the deadly bug survives in exhaled air.

“People have been focused on poorly ventilated spaces and thinking about airborne transmission over meters or across a room,” said Prof. Jonathan Reid, director of the University of Bristol’s Aerosol Research Centre, the Guardian reported.

“I’m not saying that doesn’t happen, but I think still, the greatest risk of exposure is when you’re close to someone,” said Reid, the lead author of the study, which has not yet been peer-reviewed.

“When you move further away, not only is the aerosol diluted down, there’s also less infectious virus because the virus has lost infectivity (as a result of time),” he added.

A man receives a nasal swab during a test for COVID-19 at a streetside testing booth in New York on December 17, 2021.
ED JONES/AFP via Getty Images

The UK university researchers’ findings highlight the impact of short-range transmission — and stress the importance of physical distancing and masking up as the best way to avoid infection.

While still worthwhile, ventilation was deemed to be less effective, the news outlet reported.

The study determined that viral particles quickly lose moisture and dry out after they are expelled from the lungs. The particles’ pH also rises rapidly when the carbon dioxide in their environment drops, the news outlet reported.

Prof. Jonathan Reid headed the study that shows COVID-19 is 50 percent less infectious when it hits air.
The Aerosol Society

The relative humidity of the surrounding air affects how fast the particles dry out.

When under 50 percent, such as the relatively dry air in an office, the virus had become half as infectious within 10 seconds. But at 90 percent humidity, 52 percent of particles remained infectious after five minutes, dropping to about 10 percent after 20 minutes.

Air temperature also did not affect the infectivity, contradicting the widely held belief that transmission is lower during warm weather.

Infections of the COVID-19 virus have been rising in the US.
EPA/JIM LO SCALZO

“It means that if I’m meeting friends for lunch in a pub today, the primary [risk] is likely to be me transmitting it to my friends, or my friends transmitting it to me, rather than it being transmitted from someone on the other side of the room,” Reid said.

The British researchers generated minuscule particles that floated between two electric rings between five seconds and 20 minutes as the temperature, humidity and surrounding UV light intensity were tightly controlled, the Guardian said.

“This is the first time anyone has been able to actually simulate what happens to the aerosol during the exhalation process,” Reid said.

People with children sign up to receive rapid COVID-19 tests at a Long Beach Public Health Department testing site on January 10, 2022.
PATRICK T. FALLON/AFP via Getty Images

The experts noted the inaccuracy of experiments conducted by US researchers, who found that infectious virus could still be detected after three hours.

The Bristol team said the American scientists conducted their studies by spraying virus into sealed, rotating drums that do not allow them to recreate what happens when people cough or breathe.

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