Will the virus rebound after Pfizer’s covid drug is discontinued?

More research is needed to determine the optimal dose and duration of antiviral therapy for Omicron infection, and it is also of concern how contagious it is for people who experience a rebound in COVID-19 symptoms.

Anthony Fauci, the White House’s chief medical officer and director of the National Institute of Allergy and Infectious Diseases, revealed how he was doing after testing positive for the covid last month. Fauci said he experienced a rebound in symptoms after taking a standard course (5 days) of Pfizer’s antiviral drug Paxlovid.

The researchers suggest that more research is needed to determine the optimal dose and duration of antiviral treatment for Omicron infection, such as whether some people who start later on the drug need to take a longer course of the drug, not just 5 days. . In addition, it is worth paying attention to how contagious people who experience the rebound of covid symptoms are.

Fauci says symptoms worsened after positive retest

Fauci, 81, shared the process of his infection with the covid at a recent global health forum, and used his own statement to call on the government to more systematically study the phenomenon of the rebound of symptoms after the covid infection, so as to learn more about high-risk groups and whether The standard 5-day course of treatment with Paxlovid should be extended.

He said he had mild symptoms after contracting the virus for the first time, but given his age, he took Paxlovid and avoided hospitalization. After 5 days of taking the medicine, Fauci’s nucleic acid tests were negative for three consecutive days, but the nucleic acid fluctuated on the fourth day, and he was tested positive again.

Previously, a research team from Columbia University in the United States has found cases of nucleic acid “yin to positive” after the use of Paxlovid treatment was stopped, but said that these people may have no symptoms or only mild symptoms. The team collected at least 10 cases, and the study was published on a preprint website.

But in Fauci’s case, he said his symptoms got worse after he tested positive again. Based on Fauci’s symptoms, doctors prescribed another course of Paxlovid antiviral.

There is currently no solid data on whether Paxlovid’s antiviral drug withdrawal will lead to a rebound in the covid, only small cases that people have shared on social media. Paxlovid maker Pfizer previously said a study of more than 2,200 Covid-19 patients showed that this so-called “rebound” occurred in a minority and was observed in both the placebo and drug groups, so The company believes it has nothing to do with taking the drug.

Dr. Micheal Charness of the Boston Veterans Administration Medical Center worked with the Columbia University team to study cases of covid recurrence after taking Paxlovid. The researchers observed a decrease in viral load during treatment with the Paxlovid drug. But then in some people, virus levels began to climb again nine to 12 days after they first tested positive.

Chanes said it was unclear whether this rebound in viral load was related to stopping Paxlovid. But he found something different than his previous research. Among the 1,000 U.S. professional basketball players and related staff who did not take the drug between December last year and March this year, there was no rebound in the virus.

One possible explanation is that viral rebound is more common in older people with weakened immune systems. A virus expert from the Pasteur Institute told the First Financial Reporter: “This situation is actually caused by some people with weak immune systems, and the virus clearance time in the body is longer and caused by repeated fluctuations, which should be distinguished from reinfection. Come.”

Is symptom rebound contagious?

This situation where symptoms rebound and the nucleic acid test is positive again is often referred to as “returning positive”. “Fuyang” is different from “reinfection,” which means that genetic testing shows that when people get a second round of COVID-19 after stopping Paxlovid, it’s not because they’re infected with a different strain of the virus, and there’s no sign that the virus has A change or mutation that develops some kind of resistance to the drug.

“The possible explanation is that the antiviral drugs inhibited a large number of virus replication, but did not completely kill the virus, then the residual virus began to replicate after the drug was stopped, and the concentration became positive again after accumulating to a certain extent.” Academician of the Chinese Academy of Sciences, Chinese Academy of Sciences Ma Dawei from the Shanghai Institute of Organic Chemistry explained to the first financial reporter.

He believes that the infection pattern of the new coronavirus varies from person to person, and many factors may contribute to the severity of symptoms, which are also related to the load of the virus.

Another concern, experts say, is whether people who experience a rebound in these symptoms are contagious. “People who experience a rebound are at risk of infecting others, even beyond the window during which the virus is usually able to spread,” Chanes said.

In the Paxlovid cases studied by Chanes’ team, a 63-year-old man infected two family members during a relapse three days after stopping the drug.

Who may be at higher risk of symptom rebound? Why does this happen? And why do some people experience worse symptoms after rebounding? Is it contagious after symptoms rebound? Researchers still know very little about these issues.

Experts emphasize that for “Fuyang” personnel with nucleic acid Ct value ≥35, the current evidence believes that they are not infectious. In my country’s ninth edition of the covid prevention and control plan, no matter whether the “Fuyang” personnel have clinical symptoms such as fever and cough, as long as the nucleic acid detection Ct value is ≥35, there is no need to track and control their close contacts.

“For Fuyang patients, it is not recommended to be hospitalized or to enter the square cabin for isolation and observation. They can participate in work and life normally.” Professor Lu Hongzhou, president of Shenzhen Third People’s Hospital, told Yicai.com. He said that the definition of “Fuyang” is still unclear. “The time of virus clearance in immunocompromised patients, tumor and AIDS patients may be longer. During this process, the Ct value will be repeated, but this is not the case of re-infection with the virus.” Lu Hongzhou said.

Huang Ailong, president of Chongqing Medical University, told Yicai.com, “Virus infection is a rather complicated process, and the replication and clearance of the virus are affected by the interaction between the host and the virus, and there are great individual differences, so it is not ruled out that a very small number of people are infected. Virus clearance takes a longer time and recurs.”

Based on existing research, the U.S. Centers for Disease Control and Prevention (CDC) believes that a rebound in covid symptoms may be a way for some people to contract the covid, and recommends that people who have symptoms and test positive after taking antiviral drugs , the 5-day quarantine should be restarted. The isolation period can be ended after the fever has subsided for 24 hours without the use of antipyretics and symptoms have resolved. The agency also recommends that people continue to wear masks for 10 days after symptoms resolve.

How do viruses shape our world?

As frightening as they are as agents of disease, viruses can also do wonders — shaping and evolving from the very beginning of life. About 8 percent of our DNA comes from viruses that infected our long-ago ancestors and tinkered with viral genes into their genomes; Some of these genes now play crucial roles in the early stages of embryo development and in the placenta surrounding the 13-week-old foetus (pictured above). PHOTOGRAPH BY LENNART NILSSON, TT/SCIENCE PHOTO LIBRARY (COMPOSITE OF TWO IMAGES)

Let’s imagine an earth without viruses!

We wave our wands and they disappear:

The rabies virus suddenly disappeared, the polio virus, the dreaded and deadly Ebola virus, the measles virus, the mumps virus, and the various influenza viruses, and human suffering and death were greatly reduced.

HIV disappeared, and the AIDS disaster never happened again. Nipah, Hendra, Machubo and Sinobo are all gone — never mind the messy records they once left behind. Dengue fever disappeared; All rotavirus disappeared – a great pity for the hundreds of thousands of children who die each year in developing countries. The Zika virus disappeared; Yellow fever virus disappeared; Monkey herpesvirus B, which is carried by monkeys and usually fatal when transmitted to humans, was also gone; No one gets chickenpox, hepatitis, shingles, or even the common cold anymore.

Day flower? The virus was eradicated worldwide in 1977; Now, the last samples, stored in high-security cryogenic refrigerators, have gone ghostly. The SARS virus of 2003, which marked the alarm of the modern pandemic era, disappeared. And then, of course, there is the evil SARS-COV-2 virus, the one that caused COVID-19 and whose treacherous impact on society is so intractable, so dangerous and so easily transmitted that it no longer exists.

Do you feel better about everything?

Don’t!

The situation is more confusing than you might think. The truth is, we live in a world full of viruses — of infinite variety and quantity. In the observable universe, the oceans alone may contain more virions than stars. Mammals probably carry at least 320,000 different kinds of viruses. When you add in viruses that infect non-mammals, plants, terrestrial bacteria and every other possible host, the total reaches… Countless. Not only are they vast in number, but their impact is staggering: many of these viruses have brought adaptive benefits, not harm, to life on Earth, including human life.

Without them, mankind would not be able to continue. Without them, we would not have risen from the primal muck. For example, two different lengths of DNA derived from viruses are present in the genomes of humans and other primates. The surprising truth is that without them, pregnancy would be impossible. There is also viral DNA, which is present in the genes of land animals and, more surprisingly, helps to pack and store memories in tiny protein bubbles. There are other genes from viruses that help embryos grow, regulate the immune system, and suppress cancer — important effects that are only now beginning to be understood. It turns out that viruses played a key role in triggering major evolutionary shifts. If all viruses were eliminated, as we think they are, our planet’s rich biodiversity would collapse like a beautiful wooden house, with every nail suddenly removed.

Yes, a virus is a parasitic organism. But sometimes the parasite is more like symbiosis, in which the host and the host depend on each other and benefit from each other. Like fire, viruses are a phenomenon that is neither good nor bad. They can do good or harm — it all depends on the virus, it all depends on the situation, it all depends on your reference point. They are the dark angels of evolution, good and terrible. That’s what makes them so interesting.

To understand the diversity of viruses, you need to start with the basics of what they are and what they are not. It’s easier to say they’re “not something” — they’re not living cells. Depending on whether the cell happens to be a muscle cell or a xylem cell or a neuron, one cell at a time goes through massive assembly to form sophisticated machines for building proteins, packaging energy and performing other specialized functions in order to make up your or my body, an octopus or a primrose. Bacteria, also cells, have similar properties but are much simpler. Viruses don’t.

The question of what a virus is is so complex that its definition has changed over the past 120 years. Dutch botanist Martinus Beijerinck, who studied tobacco Mosaic virus, speculated in 1898 that it was an infectious liquid. For a while, a virus was defined largely by its size — something much smaller than a bacterium, but which, like a bacterium, causes disease. More recently, viruses were thought to be submicroscopic vectors with very small genomes that could replicate in living cells — but this was only a first step towards a more appropriate understanding. (See how the virus is seen up close.)

“I will defend the paradox,” the French microbiologist Andre Lwoff wrote in an influential 1957 paper, “The Concept of viruses,” that “viruses are viruses.” This is not a clear definition, but an objective caveat — in other words, “unique to themselves.” He cleared his throat and began his complicated explanation.

Lwoff knows that it is easier to describe a virus than to define it. Each virus particle is made up of a set of genetic instructions (written in DNA or other information-carrying molecules, RNA) wrapped in a protein capsule, known as a capsid. In some cases, the capsid is surrounded by a membranous envelope, such as the caramel on a caramel apple, that protects the virus and helps it grab onto cells. A virus can replicate itself only when it enters a cell and controls a “3D printing machine” that converts genetic information into proteins.

If the host cell is unlucky, it makes lots of new virus particles, and they cause the cell to rupture, and the cell becomes debris. Such damage — such as that caused by SARS-COV-2 in human airway epithelial cells — is part of how viruses become pathogens.

But if the host cell is lucky, the virus may simply settle into this cosy outpost for the time being — either dormant or reverse-integrating its small genome into the host’s — and bide its time. This possibility has implications for genome reengineering, for evolution, and even for our sense of identity as humans, which I’ll talk more about later. Here’s a hint: in a popular 1983 book, British biologist Peter Medaval and his editor wife Jane asserted that “no virus can do any good: a virus is, as we all know, ‘a piece of protein-wrapped bad news.'” They were wrong, as were many scientists at the time, and it’s understandable that anyone whose knowledge of viruses is limited to bad news like flu and COVID-19 still accepts this view. But today, some viruses are thought to be beneficial, wrapped in proteins for genetic scheduling, good or bad as the case may be.

Where did the first viruses come from? This requires us to look back about 4 billion years, when life on Earth emerged from a hodgepodge of long molecules, simpler organic compounds and energy.

Suppose some long molecule (probably RNA) starts replicating. As these molecules — the first genomes — reproduce, mutate and evolve, Darwinian natural selection will begin here. Seeking a competitive advantage, some molecules may have found or created self-protection within membranes and walls, giving rise to the first cells. These cells split into two by fission to produce offspring. They also divide in a broader sense, differentiating into bacteria and archaea, two of the three domains of cell life. A third, eukaryotes, appeared later. It includes ourselves and all other living things (animals, plants, fungi, certain microbes) that are made up of cells with complex internal anatomy. These are the three branches on the tree of life as we now describe it.

But where is the virus? Are they the fourth main branch? Or are they a mistletoe, a parasite that floats in from somewhere else? Most versions of the evolutionary tree ignore viruses entirely.

One view is that viruses should not be included in the tree of life because they are not alive. It’s a lingering debate, depending on how you define “live.” A more interesting idea is to take viruses into a big tent called life and explore how they got in.

There are three main hypotheses to explain the evolutionary origins of viruses, which scientists call virus primacy, virus escape, and virus reduction. The idea of virus primacy is that viruses predate cells, somehow assembled directly from a hodgepodge of primordial elements. The escape hypothesis postulates that a gene or piece of a genome leaks out of a cell, gets encamped in a protein capsid, and then starts “idling around” until it finds a new niche to start parasitising. The reduction hypothesis suggests that viruses originate in cells that become smaller under competitive pressure (easier to replicate if small and simple), shedding genes all the way down to a minimalist state where only the host cell can survive.

There is a fourth hypothesis, called the chimeric hypothesis, which is inspired by another class of genetic elements: transposons (sometimes called jumping genes). Their existence was derived by geneticist Barbara McClintock in 1948, a discovery that won her a Nobel Prize. These opportunistic elements achieve Darwinian success by jumping from one location in the genome to another, in rare cases from one cell to another, or even from one species to another, using cell resources to replicate themselves over and over again. Self-replication protects them from accidental extinction. They accumulate abnormally and make up about half of the human genome. According to this idea, the earliest viruses may have been created by these elements borrowing proteins from cells and wrapping their naked self in a protective capsid — a more sophisticated strategy.

Each hypothesis has its merits. But in 2003, new evidence of giant viruses pushed expert opinion in favor of the reduction hypothesis.

It is found in amoebas, single-celled eukaryotes. The amoebas were collected from water in a cooling tower in Bradford, England. Some of the amoebas have mysterious spots inside them that are large enough to be seen with a light microscope (viruses are generally so small that they can only be seen with an electron microscope), and they look like bacteria, but when scientists tried to examine the bacterial genes inside, they found nothing.

Finally, a team of researchers in Marseille, France, infected other amoebas with the stuff, sequenced and identified its genome, and named it Mimivirus because it mimics bacteria, at least in terms of size. It’s huge in diameter, bigger than even the smallest bacteria. Its genome is also large for a virus, at almost 1.2 million bases, compared with 13,000 for influenza and 194,000 for smallpox. (DNA, like RNA, is a long molecule made up of four different molecular bases, These bases are written with the first abbreviation instead. It’s an “impossible” virus: essentially a virus, but too big, like the four-foot wingspan of the newly discovered Amazon butterfly.

Jean-michel Claverie is a senior member of the Marseille research group. The discovery of Mimivirus “caused a lot of trouble,” he told me. Why is that? Because genome sequencing revealed four very unexpected genes — genes that encode enzymes that are thought to be unique cellular genes that have never been seen before in a virus. Claverie explains that these enzymes are among the components that assemble amino acids into proteins through translation of the genetic code.

As for the discovery of these “fancy” enzymes that are usually active in cells, Claverie said, “so the question is: what does a virus want when it has cells it can dominate?”

What on earth? The logical inference is that the Mimivirus keeps them as reservations because its lineage stems from the cell’s genomic reduction.

Mimivirus is not an accident. Similar giant viruses were soon found in the Sargasso Sea, and the early name became a genus. Mimivirus, which contains several giant viruses. Then the Marseille team found two more behemoths — again, amoeba parasites — one from shallow Marine sediment off the coast of Chile and the other from a pond in Australia. The two “parasites” are twice the size of mimiviruses and even more abnormal, and are assigned to a separate genus. As they explained in 2013, Claverie and his colleagues named it Pandora virus because “further research on them was expected to surprise.”

Claverie’s senior co-author on the paper is virologist and structural biologist Chantal Abergel (who is also his wife). “They’re challenging — they’re my baby,” Abergel told me with a tired smile about Pandora. It’s hard to tell what they are, she explains, these creatures are so different from cells, so different from classic viruses, carrying many genes that have never been seen before. “All of this makes them both fascinating and mysterious.” For a while, she called them NLFS (New Life-Forms) : New life forms. But based on the observation that “they weren’t replicating by fission,” she and her colleagues realized they were viruses — the largest and most puzzling viruses ever discovered.

These findings emboldened the Marseille team to propose a variant of the “reduction hypothesis.” Maybe the virus did originate from the shrinking of an ancient cell, something that no longer exists on earth. This “ancestral protocell” may differ from — and compete with — the universal common ancestor of all cells known today. Perhaps these protocells lost their competition and were shut out of all environments where life could be free. They may have survived as parasites on other cells and shrunk their genomes, becoming what we call viruses. In the realm of lost cells, only viruses may be left, like the giant rocks of Easter Island.

The discovery of giant viruses inspired other families

Mosquitoes chasing and biting are actually a danger signal!

In the vast crowd, why do mosquitoes “bite” you? It turns out that unique body odor may be the reason why you continue to be attractive to mosquitoes.

‍On June 30, a new study published in the journal “Cell” by Professor Cheng Gong’s team from Tsinghua University verifies the above point of view. People or animals infected with dengue virus are more favored by mosquitoes. On this basis, the team also proposed a strategy that promises to prevent outbreaks of mosquito-borne diseases…

The threat of infectious diseases is huge

As soon as summer arrives, mosquitoes will follow.

This annoying creature not only brings endless noise and itching to humans, but also spreads a large number of mosquito-borne viruses, causing widespread infectious diseases (including malaria, yellow fever, dengue fever, etc.). Worldwide, nearly one million people die from it every year.

Dengue virus and Zika virus are both common mosquito-borne viruses.

Dengue fever caused by the former is one of the most widespread viral infectious diseases in the world. It is mainly carried by the Aedes mosquito and spreads in tropical (and occasionally subtropical) regions, causing rashes, fever and pain in mild cases, bleeding and even death in severe cases. According to the National Institutes of Health (NIH), more than 50 million cases of dengue fever occur around the world each year, killing about 20,000 people, mostly children.

The latter, which host another mosquito of the same genus, are relatively less likely to cause serious disease in adult populations. However, it is inextricably linked to severe birth defects in newborns. A recent Zika outbreak in South America has caused thousands of infected pregnant women to give birth to microcephaly babies.

For a long time, mankind has made unremitting efforts to prevent mosquito-borne diseases. However, due to the special infection mechanism of the virus, the relevant vaccine has not yet come out.

It is for this reason that clarifying the mechanism of the rapid spread of mosquito-borne viruses and taking effective blocking measures has become the top priority.

Locate infected people by smell

The continuation of the virus relies on the continuous two-way transmission between humans and mosquitoes. In other words, if mosquitoes always choose to “take blood” from uninfected people to eat, the virus will have a hard time surviving.

Mosquito-borne virus transmission cycle.

The research team speculates that the reason why mosquito-borne viruses spread quickly and are difficult to eradicate is most likely because mosquitoes have a way to accurately locate infected people in the vast crowd. They then compared dengue-infected mice with healthy mice and found that mosquitoes did prefer to infect mice.

But why? After digging deeper, the team focused on a volatile molecule called acetophenone.

It turned out that whether mice or humans, after being infected with dengue virus, the content of acetophenone molecules in their odors increased significantly. This molecule can activate the mosquito’s olfactory nervous system, allowing the mosquito to “hear the news” and lock on to the target and run immediately. After applying different concentrations of acetophenone to human arms, the researchers also determined that the higher the concentration of acetophenone, the more attractive the arm was to mosquitoes.

This shows that changing the odor of the host is a necessary means for mosquito-borne viruses to improve their own transmissibility.

New Ideas for Prevention and Control of Mosquito-borne Infectious Diseases

Where does acetophenone that makes mosquitoes “fascinated” come from?

It turned out that it is a metabolite of microorganisms (genus) on the skin surface. Further studies have shown that infection by dengue virus and Zika virus inhibits an important immune factor in the skin-antibacterial peptides, thereby promoting habitation Such microorganisms on the body surface proliferate in large numbers.

This regulatory mechanism helped the research team find the inspiration for blocking the large-scale epidemic of mosquito-borne diseases – as long as the expression of antimicrobial peptides is restored, the growth of Bacillus dermoides will be controlled, the acetophenone will be reduced, and the mosquitoes will not be affected. Take special interest in the infected again.

In other words, the circulation of the virus will also be interrupted.

So, is there any drug that can achieve the above effect? After trial and error using a mouse model, isotretinoin, a vitamin A derivative, offers a glimmer of hope. When mice infected with dengue virus and Zika virus were fed isotretinoin, their expression of antimicrobial peptides returned to normal and the release of acetophenone was inhibited.

However, whether vitamin A drugs are equally effective in humans remains to be further verified. At present, the research team has started to prepare for the next stage of work. It is believed that in this difficult and difficult “human-mosquito war”, human beings will win the final victory.

covid raging, Neanderthals “back the blame”

According to foreign media reports, James Davis, associate professor of genetics at the Radcliffe Department of Medicine at the University of Oxford, UK, said that the possible source of susceptibility to the virus in the lungs of modern humans is a tens of thousands of years ago between Neanderthals and early humans. “Romantic Encounter”, assuming that such interspecies mating and genetic mutation inheritance does not occur, modern humans will be more resistant to the new coronavirus, and the number of deaths will be greatly reduced.

Neanderthal-derived genes are said to appear in modern humans, and one of them, LZTFL1, is believed to have a unique effect on lung cells.

Lung cells with the LZTFL1 gene produce an important protein on the surface that the coronavirus can attach to and spread through the lungs, causing transmissible and deadly damage. This gene variant is more common in people of South Asian descent.

Genome analysis finds monkeypox virus mutates unusually fast

A new study published in Nature Medicine provides the first robust genomic analysis of the monkeypox virus that is currently spreading around the world. The study traced the virus to the 2017 monkeypox outbreak in Nigeria and showed that it rapidly produced an unusually large number of mutations that may be linked to increased human-to-human transmission.

In early May, a British resident who had recently returned from a trip to Nigeria was confirmed to have monkeypox. By the end of the month, dozens more cases had been detected around the world, from Spain, Germany and France to Australia, Mexico and the United States.

The breadth of this spread is unprecedented. Although monkeypox is endemic in parts of Central and West Africa, it has never before spread widely around the world, and scientists quickly began studying the virus’ genome to understand where it came from and how it might differ from what has been seen in the past .

Led by a team of scientists in Portugal, the new study looked at 15 different virus samples from infected people. The first genomic link found in the study was related to clusters of monkeypox cases identified in Israel, Singapore and the UK in 2018 and 2019.

These cases were all previously associated with returning travellers from Nigeria, and the genomic association was further traced to the 2017/2018 monkeypox outbreak in Nigeria.

Perhaps the most unexpected finding of the new study is the revelation that the current monkeypox strain appears to have undergone an unusually rapid period of mutation. The project’s lead researcher, João Paulo Gomes, said that one would normally only expect to see the virus accumulate a few new mutations a year, but the iterations currently circulating appear to contain around 50 new mutations.

“Considering that this 2022 monkeypox virus may be a descendant of the 2017 Nigerian monkeypox virus, we would expect no more than five to 10 additional mutations (compared to the imported virus in 2018-2019), while Not the 50 or so mutations observed,” Gomes said in an opinion piece for vaccine charity Gavi.

The prevailing assumption is that between 2019 and 2022, the virus has circulated undetected in an endemic country for several years. The current global outbreak is likely to originate from a single source and then be amplified by one or more superspreader events in early 2022, leading to widespread mass transmission that was subsequently detected in April and May.

In an interview with MedPage Today, Gomes said many of the mutations detected so far are related to human immune system proteins. This suggests that the virus may have rapidly adapted to human-to-human transmission.

Gomes told MedPage Today: “The multiple mutations we see in human-to-human transmission in 2022 affect proteins involved in the human immune system, so it could mean an adaptation process in humans. And, yes Yes, it appears to be occurring faster than expected, which is also consistent with the observation that 2022 (strain) is too mutated compared to its ancestor.”

Hugh Adler, of the Liverpool School of Tropical Medicine, said the new study highlights how little we know about the genetics of monkeypox, a virus that has been circulating for more than 50 years. Adler also stressed that it’s too early to know what the new mutations cited in the study mean for transmission or disease severity.

Adler explained: “The authors describe an unexpectedly high number of mutations in the virus, but their impact on disease severity or transmissibility is unclear. We did not find clinical disease severity in patients diagnosed in the current outbreak. any changes.”

As of June 24, 2022, more than 4,100 monkeypox cases have been reported in about 50 countries. The World Health Organization (WHO) recently convened an emergency advisory group to assess the global situation.

While the panel did acknowledge the “urgent nature of the event,” it declined to recommend that WHO declare the outbreak a Public Health Emergency of International Concern (PHEIC). WHO declares a public health emergency of international concern when a new disease is identified that is spreading internationally and requires a coordinated global response to manage. There are currently two infectious diseases declared PHEIC: polio and COVID-19.

The WHO’s hesitation in declaring the monkeypox outbreak a public health emergency has been criticized by some infectious disease experts. In an interview with Science Insider, global health policy expert Alexandra Phelan questioned the purpose of the WHO’s emergency declaration policy if it was triggered so slowly when there was an apparent spread of a new infectious disease.

“This is a global alert mechanism for public health, and I’m concerned about what it means for community transmission to wait a few weeks before fully grabbing political attention,” Phelan said in an email to Science. “I think it’s very clear that it’s time to reconsider what the goals of PHEICs are and whether the standards are fit for purpose to remind the global community and fair enough in an interconnected world.”

Raina MacIntyre, an infectious disease expert who has studied monkeypox in the past, said the transmission of the new virus was “absolutely unusual”. While calling on global health authorities to do what they can to stop the spread of the virus, she speculates that COVID-19 may have played a role in this sudden outbreak.

While weakened immunity from past smallpox vaccinations may have been a factor in the increased spread of the virus, MacIntyre wondered whether SARS-CoV-2 infection compromised people’s immune responses, making them more susceptible to monkeypox infection.

“As people recover from COVID, their immune systems are compromised,” MacIntyre wrote in an article for The Conversation. “As a result, people who have had COVID may be more susceptible to other infections. We’ve seen the same with measles infections. This weakens the immune system and increases the risk of other infections for the next two to three years.”

The new study was published in Nature Medicine.

What causes HPV virus

  1. The cause of HPV virus
  2. Viruses are everywhere in our lives, they can be lurking in the air, on objects, or even in your body.
  3. Are you thinking now, if there is a virus in the body, why am I not sick? That’s because there is a strong defense system hidden in our body – the immune system. The immune system can remove the viruses that are trying to harm us and prevent the virus from doing bad things in the body, but the immune system is not omnipotent. When the immune system is weakened or the autoimmune system is weakened for some reason, it is because the number of viruses is too much, and the immune system cannot eliminate the virus, which will cause us to get sick

How is the HPV virus spread?

Existing clinical studies have found that the HPV virus is mainly transmitted in five ways. (1) Sexual transmission; (2) Skin contact transmission; (3) Indirect contact transmission, such as clothing, daily necessities, etc.; (4) Iatrogenic transmission, infection caused by improper handling by medical staff; (5) Mother-to-child transmission, fetal transmission Infection through the birth canal during natural childbirth. The most important one is sexual transmission. Because most women are infected with HPV, it is sexually transmitted, so when you have sex in the usual room, you should know whether your sexual partner is infected with HPV virus.

Quantitative monitoring of new coronavirus antibodies with only one blood glucose meter

The blood glucose meter also has a new function-quantitative monitoring of new coronavirus antibodies. Maybe in the near future, we can use a blood glucose meter at home to complete the quantitative monitoring of new coronavirus antibodies without going to the hospital. How is this achieved? Recently, scientists have developed a new fusion protein and successfully combined it with human immunoglobulin G to quantitatively read the level of new coronavirus antibodies in the human body by measuring the amount of glucose produced.
Rapid diagnosis plays a vital role in mitigating the current global COVID-19 pandemic and preventing the large-scale spread of infectious diseases in the future. How to enable more people, especially vulnerable groups, to enjoy safe and universal medical services through rapid, accurate and low-cost diagnosis has become a global issue. Among them, the development of simple, cost-effective and widely applicable detection equipment is also a top priority. Taking the detection of novel coronavirus antigens as an example, the current standard detection method is the enzyme-linked immunosorbent assay (ELISA). Commercial ELISA instruments include portable instruments (eg, manufactured by Samsung, Alere, etc.) and high-throughput, multiplexed clinical analyzers (eg, manufactured by Luminex). However, ELISA requires expensive high-quality optical equipment to achieve the accuracy of antibody measurement, which hinders the application of ELISA in some general hospitals and laboratories; even for ELISA that has been put into use at the point of care, The vast majority are also limited to qualitative measurements. Based on the application defects of the above-mentioned ELISA, it is imminent to develop a simple, cost-effective quantitative detection scheme.
Recently, researchers from Johns Hopkins University (Johns Hopkins University) published a report entitled “Antibody–Invertase Fusion Protein Enables Quantitative” in the Journal of the American Chemical Society (JACS). The paper “Detection of SARS-CoV-2 Antibodies Using Widely Available Glucometers” shows the possibility of using blood glucose meters to quantitatively detect SARS-CoV-2 Antibodies. https://pubs.acs.org/doi/10.1021/jacs.2c02537
Research brief
01
More recently, invertase-mediated sucrose conversion has been used in molecular diagnostics; however, conjugating the invertase to a detection molecule (eg, a detection antibody) is by no means trivial. Previously, some studies avoided direct attachment of the detection antibody and invertase by coupling the detection antibody and invertase to the same nanoparticle; there were also studies using streptavidin as an intermediate between biotinylated antibody and biotinylated invertase to make the two form a complex. However, these approaches yield very low coupling efficiencies.
In this study, the researchers designed a genetic fusion protein consisting of two invertase molecules and an anti-human immunoglobulin G antibody (anti-hIgG) through genetic fusion. This novel fusion protein overcomes the problem of inefficient chemical coupling between invertase and detection molecules, and retains the binding affinity and catalytic activity of constitutive proteins, and can be used as an accurate reporter gene for immunoassays.
Research key point 1: Design and purification of “anti-human immunoglobulin G antibody (anti-hIgG)-convertase fusion protein”
Four kinds of “anti-human immunoglobulin G antibody (anti-hIgG)-invertase fusion proteins” (hereinafter referred to as Ab+Inv) were produced in the study. The positions and lengths of the peptide linkers to the two invertase molecules differ. These four classes of fusion proteins are all based on anti-hIgG HP6017, an antibody that binds the Fc domain of the human IgG isotype, and were produced by transient transfection of human embryonic kidney (HEK) 293F cells.
Research key point 2: Verify the binding of the new fusion protein (Ab+Inv) to human immunoglobulin G (human IgG)
To demonstrate that this novel fusion protein (Ab + Inv) retains binding to the target antigen (ie, human immunoglobulin G), biolayer interferometry was performed. It was found that compared with unfused antibody (human IgG), the four types of fusion proteins showed similar binding properties to human IgG. Among them, two types of binding proteins showed slightly higher affinity.
Research key point 3: Verify the catalytic activity of the new fusion protein (Ab+Inv)
To determine whether the fusion protein retained the catalytic activity of the component invertase enzyme, a commercial glucose meter was used to perform a glucose inversion assay—incubating the fusion protein with a specific concentration of sucrose to measure post-culturing glucose production Level. The assay showed that the enzymatic activities of the four fusion proteins were almost the same as that of the unfused invertase, and their enzymatic activities were not affected by their binding to human immunoglobulin G.
Research key point 4: Development and application of SARS-CoV-2 antibody detection kits
To demonstrate the diagnostic potential of the fusion protein, the researchers chose a strip-based assay because it is suitable for point-of-care use and meets the goal of cost-effective detection. We accessed confirmed negative and positive patient blood samples from institutional biorepositories and obtained two blinded training sample sets: TS1 contained six confirmed negative patients and six confirmed positive patients. TS2 consisted of 90 longitudinal samples (collected over time) from seven hospitalized patients with confirmed SARS-CoV-2 RT-PCR. The research team did not know the antibody titers of the two TSs until the researchers cross-checked commercial ELISA measurements.
The test strip of this strip detection method has the SARS-CoV-2 spike protein, and when the test strip is immersed in a sample of a COVID-19 patient, the patient’s SARS-CoV-2 antibody binds to the spike protein. This was followed by a washing step – the strip was exposed to the fusion protein solution for 30 minutes to allow the fusion protein to bind to the antibody captured on the strip, followed by washing. Subsequently, the strips were immersed in a 100 mM sucrose solution for 60 minutes to catalyze the conversion of invertase to glucose. Finally, the band was removed and the resulting glucose concentration was determined using a commercial blood glucose meter. Schematic: Quantitative determination of COVID-19-specific antibodies using a commercially available blood glucose meter
future applications
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The new fusion protein developed in this research has the advantages of low technology and low cost, which enables the diagnosis method based on blood glucose meter to be extended to a wider population, especially those who do not have access to advanced medical testing. It will also enhance the ability of serial testing, combining the number and diversity of people tested, to provide the high-quality data needed and help provide a clear and detailed understanding of the lifespan of immune protection resulting from vaccination and natural infection. In addition, this technology may be applied to the prevention and detection of cancer and autoimmune diseases—that is, replacing SARS-CoV-2 RBD with cancer diagnostic antigens or self-antigens of autoimmune diseases, so as to quantitatively detect related antibodies , beneficial for immunity testing, disease control, and longitudinal monitoring of progression.

British media falsely accuse Tedros of implying that the new coronavirus came from Wuhan

When asked by a reporter, the British Mail on Sunday, citing sources, reported that WHO Director-General Tedros Adhanom Ghebreyesus recently revealed to senior European officials privately that the most likely source of the new coronavirus was the Wuhan laboratory leak. Comments?

Wang Wenbin said that the WHO Secretariat has made clarifications to the Chinese side on the relevant reports, emphasizing that Director-General Tedros has not made any such remarks in public or in private, and the content of the reports you mentioned is completely untrue. The clerk totally disagrees with the content of the report.

“With regard to the hypothesis of laboratory leakage, China has repeatedly stated its position. The laboratory leakage is a lie concocted by anti-China forces for political purposes. There is no science at all.” Wang Wenbin said that China has invited the WHO international expert group. The joint research report also clearly reached the conclusion that laboratory leakage is extremely unlikely. Relevant media hyped up laboratory leaks in the form of “anonymous release”, ignoring the facts, with sinister intentions, and once again proving that “laboratory leaks” are completely political maneuvers by relevant parties to smear China, hinder scientific traceability, and undermine the overall situation of international anti-epidemic cooperation. alley.

Wang Wenbin pointed out that at present, there are more and more clues in the international scientific community, pointing to the global scope of the source of the virus. The U.S. government has so far failed to provide convincing answers to important questions such as when the new crown pneumonia epidemic first broke out in the United States, and has not responded to the legitimate concerns of the international community regarding the highly suspicious activities of laboratories at Fort Detrick and the University of North Carolina. If you must conduct research on laboratory problems, you must first check highly suspicious laboratories such as Fort Detrick and the University of North Carolina in the United States.

Wang Wenbin said that if relevant parties are really concerned about the issue of tracing the origin of the new coronavirus, they should pay attention to why the United States has not responded positively to the questions of the international community so far, and called on the United States to open relevant laboratories for the international community to investigate and support and cooperate with the research on the origin of the new coronavirus with practical actions. .

US nuclear submarine found virus

According to media reports, four Navy special forces were confirmed to be infected with the virus at Kitzep-Bangor Base, one of the major nuclear submarine bases of the US Navy in the United States. For training purposes, these soldiers will use U.S. submarine special operations small submarines, so it is suspected that they may have had contact with nuclear submariners. to infect the virus.

According to reports, the USS Tennessee nuclear submarine infected with the virus has been at sea for 119 days and has just arrived at the US Kitzep-Bangor nuclear submarine base for rest. The virus infection was discovered on about April 10.

The U.S. Navy “Ohio” class ballistic missile submarine “Tennessee” (SSBN734) is a strategic nuclear missile submarine that the U.S. Navy mainly participates in on strategic duty. It can carry 24 submarine-launched Trident 1 nuclear intercontinental missiles, which is also the most powerful on earth. nuclear weapons. This kind of strategic nuclear submarine is at sea most of the year, even when it is close to the dock, it will have very strict protection.

Not only are the decks guarded by armed sentries in body armor, but there are specially trained dolphins and sea lions patrolling underwater, making the submarine inaccessible to any hostile divers.

U.S. sailors once said that nuclear submarines entering the port for rest are 100 times more tiring than patrolling the sea, because they have to make all preparations for going to sea again within 35 days. Generally speaking, U.S. nuclear submarines will perform missions at sea for 3 months, and then rotate. A nuclear submarine has two groups of blue and gold personnel, and it is rotated about once every 100 days.

Modern U.S. submarines provide three meals a day for their crews when they go to sea without supplies for weeks or even months. Sysco Food Delivery feeds the submarines of the Pacific Fleet, while another company feeds the submarines on the East Coast of the United States.

Well, if the submarine has been out at sea for 119 days, as said on social media, then he was out at sea on December 14, 2019. In other words, in fact, the sailors on this nuclear submarine were infected in December last year. Later, after returning to the base on April 10 this year, it was infected with the members of the Naval Special Forces who participated in the training of the nuclear submarine.

Because the physical fitness of the nuclear submarine sailors was relatively good, and the virus toxicity was relatively weak at that time, it lasted for more than 3 months. Of course, it is also possible that the personnel who supplied supplies for the nuclear submarine infected the members of the nuclear submarine. But no matter what, the virus has been contagious in the U.S. Navy for a long time.

You know, the USS Theodore Roosevelt departed from the west coast of the United States, and now infected people have also been found at the San Diego Naval Base on the west coast. And according to the minimum standard, the U.S. nuclear submarine is rotated every 70-80 days, and this nuclear submarine has already gone to sea in January.

We can see that the truth is slowly emerging. U.S. intelligence agencies had already issued reports in November 2019 warning of a “virus catastrophe”. A November 2019 intelligence report from the U.S. Military Center for Medical Intelligence (NCMI) detailed concerns about the novel coronavirus pandemic.