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When scientists race to track metamorphosed viruses, Covid mutants multiply

With the flood of new genome data, the Los Alamos laboratory had to upgrade its servers to handle the incoming data. At the same time, Korber conducts Zoom calls 4 times a week with experts from all over the world to develop criteria to determine when the mutation is enough to cause people's attention in order to conduct detailed laboratory follow-ups on how it affects the vaccine.

Top scientists discovered a key mystery early on, and that is what kind of virus the coronavirus will prove to be. So far, it looks more like the flu, it has been deformed and needs to be re-vaccinated every year instead of measles. Measles is a virus that is not easily mutated, and a vaccine can last a lifetime.

"Does this mean we need to make a new vaccine every year?" said Paul Duprex, head of the University of Pittsburgh Vaccine Research Center. "we do not know."

On the one hand, the effective rate of the Covid-19 mRNA vaccine is more than 90%, which is much higher than the 60% flu vaccination efficiency in a bumper year. But vaccine manufacturers Moderna Inc. and Pfizer Inc. and their partners BioNTech SE did not seize any opportunities. Just in case, they have started an enhanced injection test against B.1.351, which was first discovered in South Africa.

When the virus replicates and replicates its genome, the error spit out a long string of RNA or DNA "letters" that determine how the virus protein develops. Many errors have no effect or even make the virus unsuitable for use. But a small part of these changes can give the virus an advantage, make it more infectious, or have the ability to evade the immune system.

The HIV virus is notorious for its rapid mutation rate. In contrast, the mutation rate of SARS-CoV-2 is much slower, partly because the proofreading enzyme limits the change. However, with more than 125 million infections worldwide, certain errors are bound to be missed.

Researchers at the University of Pittsburgh found that at the same time, the virus has found a mechanism to avoid its proofreading mechanism. Instead of changing individual RNA letters, it deletes groups of several letters at a time, which obviously weakens the virus's natural spelling check system's ability to see changes.

74 days of competition

Some initial deficiencies were found in an immunocompromised cancer patient treated at the University of Pittsburgh Medical Center. The patient died after a 74-day round of treatment with Covid-19. Duprex of the University of Pittsburgh pointed out that during that period, there were multiple deficiencies in evasion immunity, and he reported the absence in this cancer patient in November.

Du Perex said: "If the damn thing is gone, you won't be able to repair it."

What makes the future of SARS-CoV-2 so unpredictable is that the evolution of the virus is like a three-dimensional chess game. It is not only the individual mutations that are important, but the order and combination of their occurrence is also important. Mark Zeller, a scientist at the Scripps Research Institute in San Diego, said that a single mutation may change the virus in subtle ways, thereby changing the effects of other viruses.

Shared mutation

The B.1.351 strain that is common in South Africa and the P.1 strain that has been hit hard in Brazil have several mutations in the spike protein, which uses the spike protein to get them into the cell. This includes the D614G mutation (which makes the spikes more stable) and the E484K mutation (which is thought to reduce the ability of certain antibodies to bind to the spikes) discovered by Korber.

But so far, due to reasons that are not fully understood, at least in laboratory tests, it seems that the B.1.351 vaccine has a greater impact on Pfizer and Moderna's vaccines.

Overall, the record of virus elimination is poor, with smallpox being the main example. Although some people have made efforts to eliminate polio, there is even polio in some countries. Jesse Bloom, a researcher at the Fred Hutchinson Cancer Research Center who studies virus evolution, said that this does not bode well for the current virus.

Bloom said: "Vaccination will make this epidemic lose its advantage in a very substantial way." "But I don't think we will eradicate SARS-CoV-2."

Bloom predicts that the virus needs enough mutations to completely escape the existing vaccine, which will take "several years." He said that of the approximately 100,000 single-letter mutations in the virus, less than 1% of the virus may help the virus evade antibodies.

Hopeful scene

Although the virus continues to evolve in the short term, one of the most promising scenarios is that it may take major actions to evade the antibodies that make current vaccines work. In this case, the number of viruses that can mutate and remain suitable for invading our cells may be practically limited.

Shane Crotty, a researcher at the La Jolla Institute for Immunology, believes that the spike protein must maintain a shape so that it can effectively target its human receptor.

He said: "There are no infinite possibilities." "It's like putting a foot on a shoe. It must still be basically the correct shape and size, and it must still be recognized as a shoe."

Nonetheless, evidence from other common cold coronaviruses suggests that over time, they mutate to evade the immune system.

In a recent study, Bloom and his colleagues compared the common cold coronavirus 229E in 1984 with the same virus that was circulating in 2016 thirty years later. Due to the mutation, 17% of the RNA letters in the key part of the spike protein that bind the virus to the cell have been replaced.

In order to test the significance of this on human immunity, they obtained blood samples from patients that could neutralize the 1984 virus strain from the 1980s. These people were probably exposed to the 1984 virus and developed protective antibodies against the virus.

Fading protection

When the researchers tested the samples against the 229E virus strain that appeared in the 1990s or later, the protective effect was weakened: only 2 of the 8 blood samples were able to neutralize the 2016 strain, and these two samples were resistant to the latest virus. The activity of the virus is greatly reduced.

This provides some hints for possible future changes after sufficient time. Bloom said in an interview: "It is clear that human coronaviruses will undergo a large amount of antigenic evolution."

However, it is not clear whether the virus can retain its ability to cause serious diseases, because it will mutate and more people will be immune through infection or vaccines.

In a study published in the journal Science in January, disease modelers at Emory University found that the key factor is whether protection against severe illness lasts longer than protection against mild or asymptomatic reinfection. Much, and mild or asymptomatic reinfection is a typical coronavirus that causes the common cold.

According to Jennie S. Lavine, a postdoctoral researcher at Emory University, although this research was conducted before the current variant appeared, its basic conclusions still hold true.

Lavin, the lead author of the paper, said: "Our observations of Covid-19 at the molecular and cellular levels are not consistent with our observations of endemic coronaviruses." "Immunity is weakened, but not everything fades quickly. "

(Except for the title, this story has not been edited by NDTV staff, but has been published through a joint feed.)

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