Economists explain-is SARS-CoV-2 evolving to be more deadly? | Economist explains

After first highlighting the B.1.1.7 variant of SARS-CoV-2 First discovered in southeastern EnglandBoris Johnson said on January 22 that it was more contagious than the wild-type virus, but was not fatal. After all, it seems to be related to the high mortality rate. That’s amazing.The virus Low lethality over time. Why doesn’t this virus obey the rules?

In order for an organism to replicate, it must copy the genetic material. Occasionally, errors are sneaking up and passed. Such mutations occur in animals, plants, fungi, bacteria, and viruses. Offspring with them die before breeding because they are almost always deadly. Very rarely, the error gives the advantage that the offspring help breed better than the unmutated relatives.

Viruses are dependent on the infected person, and many viruses, such as HIV, Ebola, and the original SARS, usually become more infectious only after they have been infected throughout the body. At that point, the host’s cells are under widespread attack, the immune system is working hard, and the carrier feels exhausted and terrible. From an evolutionary point of view, if this period of extreme infectivity is withdrawn for as long as possible, the virus benefits to give more time for its offspring to spread. Killing a host suddenly limits the virus’s potential to infect others, even if the virus can spread from the corpse. Therefore, mutations that reduce the lethality of the virus are often preferred by natural selection.

However, this is not a factor for SARS-CoV-2, as it makes people most infectious when the virus first manifests and weeks before it is likely to die from complications. If you die a few weeks after becoming highly infectious, it has little effect on the evolutionary trajectory of the virus. Therefore, just as accidental mutations make it less fatal, accidental mutations are more likely to appear in the genetic code of the virus that makes it more deadly.

B.1.1.7 and several other variants, including those recently identified in California, are widespread because they carry mutations that change the tools the virus uses to invade cells. I will. SARS-CoV-2 uses spikes or “S” proteins to attach to cell surface receptors and, when activated, cause the virus to inject genetic material. The mechanism remains ambiguous, Peplomer changes Helps B.1.1.7 and other variants enter the cell. One effect is that they are more infectious.

It is also a mystery how B.1.1.7 ended up with both a mutation that makes it more lethal and a mutation that makes it more infectious. Perhaps two separate genetic alterations occurred independently in one infected individual, but this is unlikely. These two mutations were not found in individual virus strains prior to B.1.1.7. If a variant is detected, it is unlikely that two variants of the virus, each with one of the two mutations, integrated the genetic information into one unlucky person who was infected with both at the same time. .. More likely is a network of molecular interactions that means that the appearance of one mutation caused the appearance of another, just as dominoes knock down each other. Virologists increasingly believe that changes in only a few genes cause substantial changes in the behavior of the virus.

All new variants are more prone to mutation than the wild-type virus found in Wuhan in 2019. The coronavirus has a large genome, and its extra genetic material appears to be used to “error-check” the virus copy made internally in the host cell. Error checking probably helped the virus endure in bat populations for centuries in the face of valuable little resistance. We are now facing extreme resistance by moving to a new species that imposes blockades, masks, and humans. vaccine, The error checking component of the viral genome is not very valuable. Instead, what is chosen is the ability to mutate itself. More domino-like mutation cascades may be preserved.