Monthly Archives: April 2022

An article published in the April 26 issue of the journal Nature describes a series of studies by scientists on deer herds infected with the novel coronavirus, including how the virus enters the deer and occurs when the virus spreads between deer herds. and what risks these infections may pose to other wildlife and humans.
Testing deer for COVID-19 is slightly different than testing humans with nasopharyngeal swabs. Deer have long nasal passages, says Andrew Bowman, a veterinary epidemiologist at Ohio State University. “Usually we run out of cotton swabs before we get anything on [a live deer].”
These problem deer often die in the back of hunter’s trucks, in meatpacking plants or in butcher shops, waiting to be made into burgers, sausages, steaks and more. For decades, researchers have worked with hunters to manage deer populations and track the spread of infectious diseases as part of routine wildlife surveillance. Recently, scientists have also looked for the novel coronavirus that infects humans in deer.
Wearing masks and gloves, the researchers wiped the mud and grass around the deer’s nostrils and inserted cotton swabs to test for viral RNA. Blood is then collected to check for antibodies against the virus. Their work found widespread infection of North American white-tailed deer with the virus, with hundreds of infected animals in 24 U.S. states and several Canadian provinces.
Deer are widely distributed in North America. Nearly 30 million deer live in the United States, and several million live in Canada.
Variations in the virus that researchers find in deer are often consistent with those circulating in people who live nearby, but some studies suggest that SARS-CoV-2 in the wild may have mutated into new evolutionary pathways. It is unclear whether the virus spreads in long chains in deer, or whether deer-to-human transmission could trigger an outbreak. But researchers are increasingly concerned that these animals could serve as reservoirs for the virus, the source of unmanageable outbreaks that could breed new variants. Some researchers believe that highly contagious variants of Omicron linger in animal hosts for a while before appearing in humans.
Infected deer have so far not been terribly ill, but they could spread the virus to domestic animals or other potentially more vulnerable wild animals. “Once a virus enters a wild animal, there is basically no way to control it,” said Marietjie Venter, a medical virologist at the University of Pretoria in South Africa.
multifaceted outbreak
Since the outbreak of the covid, researchers have been worried about wildlife infection. To carry out their surveillance work, they started with the ACE2 receptor, a protein in host cells to which viruses normally bind to enter cells. Animals with ACE2 receptors similar to those in humans are considered at risk of infection. Teams around the world are experimenting with infection in these animals, including cats, deer mice (Peromyscus maniculatus), raccoon dogs (Nyctereutes procyonoides), and white-tailed deer, to see if they are susceptible and spread the infection.

In early January 2021, U.S. Department of Agriculture (USDA) researchers found that fawns in captivity could be infected with the novel coronavirus, shedding the virus through nasal mucus and feces, spreading the infection to other fawns in adjacent enclosures. Within a week, the animals began to develop antibodies against the virus, but no severe disease was found in the herd.
William Karesh, chair of the Paris-based OIE wildlife working group, said the findings were “somewhat surprising” because other ungulates, such as cattle, sheep and goats, are highly susceptible to infection. quite strong resistance.
Thomas DeLiberto, the coronavirus coordinator for the U.S. Department of Agriculture’s Animal and Plant Health Inspection Service Wildlife Service in Colorado, and colleagues collected 385 samples from deer between January and March 2021. About 40% of the samples contained antibodies to the novel coronavirus. In a preprint in Nature last July, the team first reported the finding, suggesting that deer had been exposed to the virus, but it was unclear if it was a one-time exposure or if the virus had already started spreading in the animals. It is also possible that these antibody production is the result of infection with other coronaviruses in the deer.
The results have prompted new deer sampling across North America to begin, and an urgent release of the results of sampling projects that have been undertaken.
In 2020, the first year of the COVID-19 outbreak, scientists began collecting nasal swabs and blood samples from deer to test for the virus using polymerase chain reaction. Until December 2020, “all we got were negative samples,” said Vanessa Hale, an animal health researcher at Ohio State University. However, between January and March 2021, she and Bowman found 129 deer that tested positive for SARS-CoV-2 RNA among about 360 animals sampled in Ohio.
Genome sequencing of more than half of the samples taken from infected Ohio deer showed similar mutations to the virus circulating in human communities across the state at the time. Since then, researchers have found positive deer in 24 of the roughly 30 U.S. states that reported sampling, as well as in the Canadian provinces of Quebec and Ontario, although Canada has a lower positivity rate of 1%-6%.
In late December 2021, researchers found a highly contagious variant of Omicron in a white-tailed deer living on Staten Island in New York City. In March 2022, a mule deer (Odocoileus hemionus) in Utah tested positive for the novel coronavirus.
However, the infection of deer with the covid virus appears to be limited to North America. “To date, despite extensive research, no one has found the virus in European deer,” said Rachael Tarlinton, a veterinary virologist at the University of Nottingham, UK.
Biological differences do not appear to explain the differences, the researchers said. “All the data on the ACE2 receptor suggest that European deer species should be as susceptible as white-tailed deer,” Tarrington said. Instead, outbreaks in North American deer appear to be the result of high deer densities and frequent human interaction with them.
“In the Americas, deer are basically in the wild or in people’s backyards,” Venter said, adding that where she works, there is much less interaction with large ungulates. “In Africa, most animals stay in wildlife reserves.”
How deer are infected by humans
How the deer got infected remains a mystery. Humans transmit pathogens in the wild, such as E. coli, the measles virus, and the protozoan Giardia. But these “spillover” situations rarely lead to sustained transmission.
Scientists speculate that direct contact, such as people petting or feeding animals with their hands, may be to blame. In North American towns and cities, white-tailed deer live close to people—living near human houses, walking the streets, and exploring college campuses. In some U.S. states, deer are raised for food, and others have rehabilitation programs for deer orphaned by car accidents. Deer in captivity may have frequent contact with humans and wild deer, and they may also escape or be released back into the wild.
But Hale said that in these cases, there may not be enough direct contact to explain the hundreds of cases identified so far, let alone the countless undocumented cases.
Another path might be via the environment. While there is no clear route for the virus to spread in humans through contaminated surfaces, deer may have contracted the virus by sticking their noses into discarded masks or by swallowing flowers and garden vegetables from which humans have sneezed. Hunters also sometimes use corn or vegetables that may be infected with the virus as bait. But Hale noted that the deer had to arrive at the right time to ingest enough virus to infect them.
In addition, the researchers speculate that contaminated wastewater may also have infiltrated the animals’ water sources. However, although many studies have found viral RNA in sewage, no infectious virus has been isolated from it. And it’s not just urban deer that get infected, the researchers say, some infected deer live in isolated areas.
According to some reports, other animals such as wild cats or wild mink may also act as vectors.
“All of these seem far-fetched until we can prove them,” Hale said. The source of infection does not have to be just one, the researchers said, and may involve multiple routes.
Can deer reinfect people?
Once a deer is infected with the novel coronavirus, there are many opportunities for the virus to spread among the wider population. White-tailed deer are very social animals, and during the breeding season, from October to February each year, bucks can walk dozens of kilometers, moving back and forth between different herds, fighting other bucks along the way. Occasionally, a female deer will also travel up to 100 kilometers to “visit relatives and friends,” returning to her usual territory in a few days or weeks. In some northern states, during periods of heavy snowfall, deer herds sometimes migrate to “deer parks” with dense trees where they may encounter other herds. During this time, the animals have been in contact with each other and may spread the virus. “There’s a lot of face-to-face contact between deer,” said Linda Saif, a virologist at Ohio State University in Worcester.
All the potential for the virus to spread has scientists concerned that deer could be the reservoir of the novel coronavirus — a permanent reservoir and a recurring source of outbreaks in other animals, including humans. Saif said that once settled in the deer, the novel coronavirus may mutate, evolve, and possibly recombine with other coronavirus genes. It could have evolved to more easily infect other herbivores, such as sheep, goats and cattle, which share pastures with deer, she said. “Once you have a single wild animal host, conceivably it’s passed on to other wild animals, even domestic livestock,” she said.
Mounting evidence supports such concerns. For example, the novel coronavirus shows signs of long-term evolution in deer. In a February Nature preprint, Samira Mubareka, a virologist at the Sunnybrook Institute in Toronto, Canada, and her colleagues report on the November and December 2021 events in Ontario. Five SARS-CoV-2 genomes of deer sampled in the province were sequenced. Compared with the original novel coronavirus, these viruses have 76 mutations, some of which lead to amino acid changes in the spike protein the virus uses to infect cells. This mutation is the key to the success of the highly infectious mutation.
In the second Nature preprint on February 9, researchers discovered the novel coronavirus alpha and delta variants in Pennsylvania deer in November 2021. The genomes of these alpha variants are different from those found in humans, and these alpha variants were found in deer months after delta variants became the dominant human-infecting variant, suggesting that alpha variants may have evolved independently in deer populations .
Mubareka and her colleagues made another unexpected discovery: a human from southwestern Ontario had a viral sequence that closely resembled the genome of the virus found in deer. Although the evidence is unclear, scientists suspect that the person may have contracted the virus from a deer.
If this is confirmed, deer-to-human transmission would be a concern. From samples taken in December and January, the researchers also found a deer infected with the Omicron variant, which also had antibodies against the delta variant.
The researchers say there is not enough evidence yet to say whether deer are breeding grounds for dangerous mutations in the virus. Karesh said he needs to see more “spillover” events — from deer to people — to call them hosts of human infection.
To really understand the situation, more sampling of animals is needed. Some researchers have begun longitudinal studies that revisit sampling sites over several hunting seasons.
In March 2021, the U.S. Department of Agriculture received a $300 million grant to investigate animals susceptible to the novel coronavirus, and researchers sampled deer in at least 27 states during the 2022 hunting season. Boto said his team plans to study footage of deer interacting with humans and other animals to quantify their interaction patterns. Another researcher said that more sampling to determine which deer are at the highest risk — bucks or females, urban or suburban deer — may provide more clues.
The scientists also plan to conduct more experimental infection studies to see if variants like Omicron and Delta behave differently in white-tailed deer, and whether other wild animals are susceptible. They might also try mixed-species studies, for example, to see if minks can transmit infections to rodents.
Mubareka said more needs to be done to track these fast-spreading incidents. “These are just early chapters,” she said.

When the community completes a round of nucleic acid screening, those infected with a high viral load are usually screened, but some infected with a low viral load will show negative nucleic acid results. Therefore, continuous nucleic acid screening is needed to dynamically detect positive infections as soon as possible.

Nucleic acid testing is an important basis for epidemic prevention and treatment. What is the accuracy rate of nucleic acid testing? Some residents think that there is no need to do nucleic acid frequently, self-test antigen is ok, can you answer?

In response, Hu Xiaobo, Director of Shanghai Clinical Laboratory Center, said at a press conference on epidemic prevention and control held on April 25 that nucleic acid test is mainly used to determine whether an individual is infected with novel coronavirus, which is a highly sensitive test method. The novel Coronavirus nucleic acid test has always been the diagnostic standard for COVID-19 in China.

The current nucleic acid detection method is mainly to extract the viral RNA from the sample, and then use polymerase chain reaction (PCR) to amplify the viral gene sequence. This method has high sensitivity and specificity. “Under ideal conditions, nucleic acid testing accuracy can reach a very high level if all the steps of sampling, transportation, verification, testing, result interpretation and reporting are accurate,” Hu said.

However, the accuracy of nucleic acid detection is also affected by relevant factors, such as the cooperation of the subject when taking samples, the temperature and time of sample storage, and the standardization of the detection process. In order to ensure the accuracy of nucleic acid test results, the laboratory will take a variety of measures, such as setting internal standards to confirm whether the sample is qualified, through indoor quality control to monitor.

Shanghai launched nine campaigns to eliminate social encounters from April 22, in which the combined screening mode of “antigen + nucleic acid” was adopted in the screening campaign.

Compared with nucleic acid tests, antigen tests are fast and easy to use, and can be used for home tests, but their sensitivity is lower than nucleic acid tests, because nucleic acid tests are exponential amplification processes that make viruses easier to detect by appropriately amplifying the concentration of virus fragments, he said.

“So if a person is in the early stages of infection and the signs are not there, then the antigen test may be negative and nucleic acid testing is needed to confirm that.” Hu xiaobo said, “The accuracy of antigen testing also depends on the standardization of individual operations. Antigen testing is not a substitute for nucleic acid testing.”

He pointed out that the recent continuous screening is based on such considerations, as there is a certain incubation period in terms of the course of novel coronavirus infection, and the viral load varies from individual to individual. When the community completes a round of nucleic acid screening, those infected with a high viral load are usually screened, but some infected with a low viral load will show negative nucleic acid results. Therefore, it is necessary to carry out nucleic acid screening for many times in order to dynamically detect positive infections as soon as possible and achieve dynamic social clearance as soon as possible.

Cover reporter Shao Meng

In the third year of the human war against the “epidemic”, the novel coronavirus has not stopped its evolution and mutation.

Since March this year, the UK Health and Safety Agency (UKHSA) has reported three recombinant strains: XF, XE and XD. The World Health Organization pointed out in the report that early estimates indicate that the XE strain is more than the current global predominant strain. Omicron BA.2 has a 10% growth advantage;

On April 11, WHO added the new sub-variants BA.4 and BA.5 of the Omicron variant to the surveillance list;

On April 12, South Korea’s Central Epidemic Prevention and Control Headquarters stated that the first confirmed case of infection with the novel coronavirus recombinant strain XL was found, and an epidemiological investigation is currently underway;

The New York State Department of Health said on April 13 local time that two new Omicron subtype variants, BA.2.12 and BA.2.12.1, were found in the state, accounting for about 80.6% of the state’s covid infections.. ….

Will the novel coronavirus continue to mutate? Does its pathogenicity decrease with the variant? What requirements does the mutated novel coronavirus put forward for vaccine development? How should we respond?

Will the mutation of the novel coronavirus continue?

The cover news reporter combed through the data of the WHO’s Cov-Lineages platform to track SARS-CoV-2 variants and found that since the outbreak of the covid at the end of 2019, there have been more than 1,600 clearly reported variant lineages. In the face of successive novel coronavirus variants, many people question: Will the novel coronavirus continue to mutate?

“The covid pneumonia virus is a single-stranded RNA virus. From a virological point of view, it is easier to mutate. As long as it has the opportunity to replicate, it will continue to mutate.” President of Shenzhen Third People’s Hospital, expert in disease prevention and control of the National Health Commission Lu Hongzhou, a member of the committee and an academician of the American Academy of Microbiology, said in an interview with a cover reporter that the virus has no mind, and the only way for it to exist is to use all the surrounding nutrients to synthesize its offspring and replicate its own “offspring”. The best way for the novel coronavirus to mutate is to stop it from replicating.

There are many variants of the novel coronavirus, but very few have become dominant strains.

Jin Dongyan, a professor and virology expert at the School of Biomedical Sciences at the University of Hong Kong, told reporters that any virus can mutate. Although the novel coronavirus is very prone to mutation, its mutation rate is actually lower than that of SARS, influenza and HIV. “From the Wuhan period to the present, there have been thousands of mutant strains and hundreds of recombinant strains of the novel coronavirus. But when we look back at the covid epidemic, most of the strains are short-lived. Many strains may even be discovered. The opportunity is gone.” Jin Dongyan said that there is survival of the fittest among the novel coronavirus strains, and only those with strong adaptability can survive.

He believes that the novel coronavirus will still mutate in the future, but from the natural law of virus evolution and development, its mutation rate cannot become faster and faster, and the infection rate cannot increase indefinitely. “The novel coronavirus is constrained by its own characteristics and changes in a ‘cage’.” Jin Dongyan said that the ultimate goal of the virus is to coexist with the host, and it will become more and more suitable for humans. But at the same time, recognize that the adaptation process is longer, and we will still be coexisting with the novel coronavirus for a considerable period of time.

On March 1, in Central, Hong Kong, citizens wore masks to travel. Photo by Xinhua News Agency reporter Lu Binghui

Will the pathogenicity of the novel coronavirus become weaker as it mutates?

As the novel coronavirus mutates, will its pathogenicity gradually weaken?

WHO Director-General Tedros Adhanom Ghebreyesus said on March 30 that existing research shows that the most likely scenario is that the novel coronavirus will continue to evolve, but as human immunity increases due to vaccination or infection, the novel coronavirus will lead to The severity of the disease decreases over time. But he also suggested a worst-case scenario: the emergence of a more pathogenic and highly contagious variant, in which protection from previous vaccination or infection would rapidly diminish .

Citing known data, Lu Hongzhou said that the novel coronavirus has been detected in 29 species of animals, which may in turn infect humans, and the virus can recombine in human cells. “There are too many uncertainties, so there is no Which scientist or theory says that the mutation direction of the virus must be from strong to weak.”

He believes that Omicron is highly contagious. Even if it has been infected in the past, it can be re-infected. It will inevitably include some elderly people or people who have not been vaccinated. The death rate may still remain high, so it must not be regarded as a “Big Flu”.

Jin Dongyan told reporters that most of the recombinant strains will die out quickly, and so far none of the recombinant strains can become the dominant strain in the world. Compared with recombinant strains such as XD, XF, XE, etc., we should be more alert to the sudden emergence of new mutants.

He said that the ultimate goal of the virus is to coexist with the host, and it will become more and more adapted to humans. The possibility of highly pathogenic variant strains cannot be said to be non-existent, but it is very low. The transmissibility may increase with the variation, but limited by its own characteristics, its transmissibility cannot be infinitely increased. Most coronavirus scholars believe that the four resident coronaviruses that only cause common colds in humans evolved from highly pathogenic predecessors, and that the novel coronavirus may also lead to the same goal in the future. As long as human beings work together to control the epidemic and reduce the chance of the novel coronavirus replicating, the chances of the virus mutating will also be reduced. With the advent of a new generation of vaccines, it remains to be seen whether the novel coronavirus will disappear from humans like smallpox and polioviruses.

The virus keeps mutating, how to deal with it?

“It’s better to get a vaccine, an effective vaccine, and a better vaccine.” When talking about how to deal with the constantly mutating novel coronavirus, Jin Dongyan repeatedly emphasized the role of vaccines. He said that the data of this round of Hong Kong epidemic has further proved the importance of vaccination. After the third dose of the vaccine, the infection rate, severe rate and mortality rate will be greatly reduced.

On April 12, the cover reporter attended the press conference of the Joint Prevention and Control Mechanism of the State Council in Beijing. At the meeting, Wang Huaqing, chief expert of the immunization program of the Chinese Center for Disease Control and Prevention, also pointed out that the latest research in Hong Kong shows that three doses of the novel coronavirus vaccine can reduce the risk of severe illness and death by more than 90%.

In addition, another new study in Hong Kong on April 8 showed that among people over 60 years old, the relative risk of death caused by no vaccination was 21 times that of those who received two or more doses.

Lu Hongzhou told reporters that in order to block the mutation of the novel coronavirus, it is still necessary to strengthen basic research. The virus is changing, but basic research on the virus will find some mechanisms that “remain unchanged”. “We can discover the mechanisms of viral immune escape, and now that we understand it, there are ways to prevent them from escaping.”

Lu Hongzhou emphasized the need to develop inhaled vaccines. “It can generate both cellular immunity and mucosal immune response where the virus invades the upper respiratory tract of the human body. The respiratory tract is the gateway for virus invasion. With immune protection at the first pass, the virus cannot enter or replicate. This is the future of vaccine development. direction.”

In addition to vaccines, Lu Hongzhou believes that the popularization and use of oral small-molecule drugs is also very important. “Basic research should be strengthened for vaccines and specific drugs. With effective vaccines and oral small-molecule drugs, the epidemic will be effectively controlled.”

How can individuals strengthen their protection against the constantly mutating novel coronavirus?

At the press conference of the Joint Prevention and Control Mechanism of the State Council held on April 12, Wu Zunyou, chief expert on the immunization program of the Chinese Center for Disease Control and Prevention, told the cover reporter that whether the virus has become a new strain, or the two viruses have become heavy in the body To compose new virus mutations, we can all “remain unchanged”. For individuals, it is necessary to implement protective measures, including wearing masks, hand hygiene, social distancing, active vaccination, etc., to deal with the capricious phenomenon of virus mutation and reduce the risk of personal infection.

After the novel coronavirus infection, the symptoms of patients vary widely, from asymptomatic to severe pneumonia and even death. The severity of the disease is closely related to inflammation in the body. Severe inflammation is the culprit that causes patients to suffer from respiratory distress and systemic multiple organ failure.

Although the severe disease rate has dropped significantly compared to previous strains during the Omicron epidemic, we still do not understand why some people become severely ill after contracting the novel coronavirus, and how the novel coronavirus ignites inflammation in their bodies stormy?

Recently, a research team from Boston Children’s Hospital unraveled the answer to this question for the first time. Surprisingly, the novel coronavirus actually infects immune cells, causing inflammatory necrosis of monocytes and lung macrophages. One process is relying on the covid antibody to play the role of “matchmaking”. The study was launched on Nature’s official website on April 6 as an Accelerated Article Preview.

The researchers analyzed and compared fresh blood samples from patients with covids and blood samples from healthy people. The results showed that in the blood of patients with covids, about 6% of monocytes are experiencing pyroptosis (Pyroptosis), also known as inflammation. During sexual necrosis, the pyroptotic cells continue to expand until the cell membrane ruptures, releasing cytokines and chemokines.

Not only that, but nearly 1/4 of lung macrophages were observed to have pyroptosis in lung autopsy specimens of COVID-19 deaths. Macrophages and monocytes have similar functions. react when.

In the early stage of infection, the substances released by these pyroptotic cells act as “alarms”, which can recruit other immune cells to the site of infection and clear pathogens in time. However, when more and more pyroptotic cells are released, inflammatory molecules are released in large quantities, and the inflammatory response is out of control. , resulting in respiratory distress and systemic multi-organ failure.

In addition, the researchers also found that the more pyroptotic cells, the more severe the patient’s symptoms. Compared with patients with mild and moderate symptoms of the covid, the blood of critically ill patients has markers of pyroptosis, including GSDMD, LDH, and IL. The levels of -1RA and IL-18 were significantly increased.

So what causes the pyroptosis of monocytes/macrophages in patients with covids?

Then, the surprising thing happened, the researchers found signs of novel coronavirus infection in these pyroptotic monocytes and macrophages – about 10% of monocytes and 8% of lung macrophages. The nucleoprotein capsid and double-stranded RNA of the novel coronavirus are present in cells.

This shows that the novel coronavirus not only entered the cell, but also tried to replicate, and these infected monocytes and macrophages all had inflammasome activation and went to pyroptosis, indicating that the direct infection of the novel coronavirus is a monocyte / The direct cause of macrophage pyroptosis!

We know that the novel coronavirus infects cells by combining the spike protein on the surface of the virus with the ACE2 receptor of the cell, like a key unlocking the door, opening the door to enter the cell. The question is, monocytes do not express ACE2, how does the virus infect it?

One point is very crucial. The researchers found in the experiment that the virus is more inclined to infect those monocytes that carry CD16 (Fc γ RIIIa). About half of the CD16+ monocytes are infected with the novel coronavirus, while the CD16- monocytes are infected with the novel coronavirus. Nuclear cells are hardly infected.

Since CD16 can bind to the Fc segment of the antibody, and then engulf those pathogens linked to the antibody, the researchers speculate that after the novel coronavirus binds to the novel coronavirus antibody produced in the body, the Fc segment at the end of the antibody is in turn absorbed by CD16 on the surface of monocytes. Capture, the cell membrane of monocytes invaginates, and the antibody and virus are engulfed into the cell, causing infection.

In order to prove that SARS-CoV-2 indeed entered monocytes through the “matching” of SARS-CoV-2 antibodies and CD16, the researchers co-cultured monocytes with an infectious engineered virus strain (icSARS-CoV-2-mNG) under in vitro conditions .

It was found that under normal circumstances, the novel coronavirus does not enter monocytes, and only when endotoxin LPS stimulation, new coronary antibodies or plasma of new coronary patients are added, monocytes will be infected by the novel coronavirus.

On the contrary, if the antibody component in the plasma of the covid patient is removed and added to the co-culture system, the number of monocytes infected with the covid virus will drop significantly. Not only that, adding a CD16 antagonist to the culture system to block the binding of the antibody to CD16 can also achieve a similar effect. It shows that the covid antibody and CD16 are indispensable in the process of the covid virus infecting monocytes.

That is to say, the covid antibody not only does not play a protective role, but instead promotes the novel coronavirus to infect monocytes and lung macrophages, causing these cells to undergo pyroptosis and an inflammatory storm, which is reminiscent of the antibody-dependent infection-enhancing effect. (Antibody-dependent enhancement, referred to as ADE effect).

The ADE effect refers to the phenomenon that after the body produces antibodies to a certain pathogen through infection, immunization or passive infusion, these antibodies assist the virus to enter the target cells, increase the infection rate, and cause aggravation of the disease.

The question is, does the covid antibody produced after vaccination also have an ADE effect?

The researchers added the plasma of healthy people who had been vaccinated with mRNA vaccine and produced covid antibodies into the co-culture system of monocytes and virus. The concentration of antibodies in the plasma of vaccinated healthy people was about twice that of patients with covid infection (6.5 ± 1.1 μg/ml vs. 3.6 ± 0.5 μg/ml), even in this case, the infectivity of the virus was not enhanced, indicating that the covid antibodies produced by the mRNA vaccine did not have an ADE effect.

So why do the antibodies in the body protect most people after being infected with the covid, while some people develop severe disease?

Previous studies have shown that the non-fucose-modified (afucosylated) of the Fc region of the antibody can promote the binding of the antibody to CD16. In the co-culture system, high concentrations (~30%) of non-fucose-modified SARS-CoV-2 antibody plasma were added to the co-culture system. Compared with the concentration of non-fucose-modified antibody plasma (~8%), the ability of the virus to infect cells was significantly enhanced, suggesting that the non-fucose modification of the Fc segment of the covid antibody is likely to be the cause of the ADE effect. Further research is needed.

This study is the first to find that the covid antibody has an ADE effect in humans, and it is likely to be the main cause of severe illness and death in patients. These antibodies promote the infection of immune cells by the novel coronavirus, promote cell pyroptosis, trigger strong inflammation, and aggravate the disease.

From this point of view, the use of pyroptosis markers in the blood of patients with covids may be able to predict disease progression, or prevent the progression of the disease from becoming severe by inhibiting the pyroptotic pathway. At present, two GSDMD inhibitors, Antabuse and Tecfidera, have entered the clinical evaluation stage for the treatment of covids ( NCT04485130, NCT04594343, NCT04381936 ), and they are expected to bring good results.

Ohio State University microbiologists found more than 5,000 new RNA viruses in seawater samples collected around the world and increased the number of phyla they classified from five to 10. This new trove of data on RNA viruses expands the possibilities for ecological research and reshaps understanding of how these small but important submicroscopic particles evolve. The study was published in the journal Science.

The team collected seawater samples and sequenced them for viral RNA by searching for genes that encode RNA-dependent RNA polymerase (RdRp). The team then used supercomputers and machine learning algorithms to build phylogenetic trees for RNA viruses, finding a total of 5,504 new Marine RNA viruses and increasing the number of known RNA virus gates from five to 10.

The researchers grouped the newly discovered virus into five newly proposed gates. Mapping these new sequences geographically shows that two of the new gates are particularly abundant.

The researchers believe that one of the five newly discovered viral gates could be the missing link in the evolution of RNA viruses that researchers have long sought, linking two known branches of RNA viruses that differ in how they replicate. The discovery fills in some of the missing pieces in the evolutionary history of viruses.

Learning more about viral diversity and abundance in the world’s oceans will help explain the role of Marine microbes in ocean adaptation to climate change, the researchers said. The ocean absorbs half of the human-produced carbon dioxide in the atmosphere, and previous work by the team has shown that Marine viruses act as “knobs” on biological pumps, affecting how carbon is stored in the ocean.

In addition, these new viruses will help scientists better understand not only the evolutionary history of RNA viruses, but also the evolution of early life on Earth.

RNA viruses can cause deadly disease, as the COVID-19 pandemic has shown. But RNA viruses also play a vital role in ecosystems because they can infect a wide range of organisms, including animals, plants and microbes. Mapping where in the world these RNA viruses live helps illuminate how they affect the organisms that drive many ecological processes on Earth. The study could also help researchers classify new viruses as their genetic databases grow.

An advocacy group for the Poor in the United States has collaborated with UN economists to produce a REPORT on COVID-19 among the Poor. The overall death rate from the epidemic in poor COUNTIES in the United States was almost twice as high as in affluent counties, the report noted. During the third wave in the United States, death rates in the poorest counties were 4.5 times higher than in the richest counties; During the most recent wave, the difference in death rates was also nearly three times greater. No wonder that in the United States, “the Novel Coronavirus is the poor man’s virus.”

There is a deliberate neglect of the poor and minorities by the US government and society, and this discrimination clearly undermines their ability to receive care. As noted at the beginning of this report, novel Coronavirus does not discriminate, but American society does. If the US government really values and protects human rights, they should value and protect everyone’s life without discrimination.

New York Mayor John Adams has tested positive for the Novel coronavirus virus, the New York City government said in a statement on Tuesday.

“Novel Coronavirus tests conducted on Mr. Adams, who developed hoarseness that morning, were positive,” the statement said. Adams, who has no other symptoms, has been quarantined and will cancel his public engagements. During the quarantine, Adams will continue to work remotely.

Adams will immediately begin taking the anti-Novel Coronavirus drug, which is available free of charge to New Yorkers, and he is encouraging eligible New Yorkers to take them, the statement said.

Dozens of people who attended a recent dinner in Washington, DC, are now reported to have contracted novel coronavirus infections.

British researchers published a study in a new issue of the Journal of Global Health, analyzing the deaths from the covid epidemic in countries and regions such as the United States and the United Kingdom, saying that the United States and Britain were considered to be the most prepared for the epidemic before the covid pandemic. countries, but the actual situation is less than expected.

Researchers at the University of Manchester in the United Kingdom analyzed data on the number of deaths from the covid in 20 countries and regions. Among them, the indicator “years of life lost” reflects the premature death caused by the covid compared with life expectancy. Calculations show that the United States has the highest overall number of years of life lost at 10,289,624, and even when calculated in proportion to the population, the United States is still at the forefront in terms of years of life lost per 1,000 people.

In terms of deaths per 1,000 people, England and Wales have the highest rate of 2.39 of the above-mentioned countries and territories. England and Wales also had the highest rate of Covid-19 deaths at 5.78 per cent of people over 90.

Researchers at the University of Manchester said the results showed that the actual situation of the United States and Britain in dealing with the covid pandemic was less than expected in previous studies. In the 2019 Global Health Security Index, the United States and the United Kingdom are considered the two most prepared countries for an epidemic or pandemic.

The researchers also pointed out that different anti-epidemic measures can significantly affect the mortality rate of some age groups. For example, when compared to Australia, which has a similar health care system, population composition and care home environment, analysis has shown that the death rate in care homes in the UK is 270 to 300 times higher than in Australia.