What to do with the many mutations in the ape smallpox genome

InChicken scientists study the spread of infectious diseases, one of which is the genetic sequence of the pathogen. But there is a drawback monkey smallpox virusThis is the reason now An unprecedented epidemic Hundreds of infections are common in some 30 countries.

DNA viruses, especially those with relatively large genomes, such as poxviruses (a family of monkeys), often accumulate mutations more slowly than RNA viruses, such as SARS-CoV-2, which produces covid-19. This means that studying these lists may be less effective in controlling how the virus spreads from person to person. There are fewer changes in the virus’s genome that could shed light on transmission chains.

However, as researchers around the world share the sequence of the current epidemic, genomes have come to an astonishing conclusion: mutations are far more numerous than expected.

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In such a short period of time, so many mutations can seem dangerous if it means that the virus is evolving to spread more effectively among humans. But scientists have another hypothesis about what these mutations say about these infections, and, in turn, what this may reveal (still a hypothesis, they emphasize, it needs further study) it is an epidemic.

Below, STAT examines some of the questions posed by the concepts of Richard Neher, a computational evolutionary biologist at the University of Basel.

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What do these lists show in terms of mutations?

Most importantly, there are many mutations in the new list. The genomes of the current epidemic share some 40 mutations with each other, which distinguishes them from their closest relatives in 2018. (The exact number of mutations varies depending on how certain changes are counted.)

According to conventional evolutionary charts, scientists expect a monkey-like virus to cause many mutations in 50 years, not four, Neher said.

“It’s a little surprising,” he said.

Why are there so many mutations?

Many mutations can be bad – perhaps because the virus has changed so much that it has become viable and has improved transmission among humans. Unlike monkeys, SARS-2 has never been considered a highly effective human-to-human transmitter.

But there may be another explanation.

We think that mutations are the result of random errors that occur during the transfer of genetic material. Some mutations have no real effect on the virus, some may actually be harmful, and some give it an advantage over other strains.

However, changes in viral genomes occur as a result of other mechanisms – and there are indications of what is going on in these monkey chains.

Many of the changes, for example, are specific exchanges in the “letters” that make up DNA, such as G and A or Sdan T. Not only that, these mutations are happening in certain parts of the chain.

“These are not just random collections of mutations,” Neher said. “These are special types of mutations.”

Here’s what might happen: Some hosts (in this case, humans) have enzymes designed to cause mutations in all the viruses they encounter as part of their immune systems. The basic idea of ​​this sabotage scheme is that if you cause enough mutations, some of them will certainly be harmful. The virus cannot reproduce and the rest is “dead part of DNA,” Neher said. It would be like rearranging the letters on your enemy’s typewriter to prevent them from being pronounced.

(There are different types of enzymes that play this role, but with the onset of monkey disease, scientists scattered in a family called APOBEC3 as the main candidate.)

The strategy is not always perfect, and some viruses may not be able to stop harmful mutations. However, these survivors carry evidence of a genetic attack in the form of known mutations, possibly less harmful or neutral ones. Mutations can occur over and over again, as in the case of monkeys. Researchers have compared these mutations to scars from a conflict with a host.

Enzyme Vs. Viral battles can explain why the virus received so many mutations so quickly. Mutations are not typical copying errors made in virus replication. They are war wounds when the host tries to fight the virus.

What do these sequences mean for this epidemic?

This accelerated evolution seems to have taken place approximately in 2017 based on the available sequence. The pattern of mutations could be evidence that the virus has since spread to low-level people. Outbreaks outside the endemic area of ​​the virus have been observed only recently, perhaps as a result of events such as festivals and the return of world travel.

One explanation, according to Neher, is “yes, it has been circulating in humans since 2017 and the level of mutation in humans is about 10 times higher. [than the virus’s normal rate]. However, this is not a copying problem, but an attempt by the hosting process. ”

It should be noted that Nigeria has been experiencing an ape epidemic since 2017, but it is still unknown where it is, including where it is. America and Europe first appeared. This was reported by Nigerian health officials they asked for international help to find out what was going on with the monkey pox, but there wasn’t much interest.

Neher said there are other possibilities to explain the mutations. It is possible that the offspring continued to accumulate mutations through this type of antiviral enzyme process before being shed back to animals and passed back to humans. Although researchers view the sequence as a suggestion that the virus has been prevalent among humans for many years, there are other potential explanations that need to be studied.

One mystery about the current epidemic is whether the virus has become contagious or has spread to people who are in close contact with many others. According to Neher, the study of consistency does not answer this question. He explained that looking at individual mutations or a combination of them, it is impossible to conclude whether they lead to functional changes or have an evolutionary advantage. (Researchers have studied epidemiological data and laboratory experiments to determine if mutations can alter the virus’s viability.)

“We don’t have a clear understanding of how this virus interacts with the host or what these individual mutations can do,” he said.

However, as the epidemic progresses and more infections are detected, scientists will have more genomes to study. This will help clarify their current hypotheses or introduce new ones in their entirety.

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