Monkeypox virus is mutating – How worried are scientists?

THE Monkey pox has spread across the globe, yet the fact that it is only transmitted by physical contact, and that it is not as deadly as scientists first feared, has acted as a “cure” for the world’s anxiety. However, a new discovery caused intense disturbance in the scientific community.

Researchers at the Minnesota Department of Health in St. Paul, who sequenced samples of the monkeypox virus a few months ago, made a surprising discovery. In a sample collected from an infected person, a large chunk of the virus’s genome was missing and another chunk had moved to a completely different point in the sequence.

Crystal Gigante, a microbiologist at US Centers for Disease Control and Prevention in Atlanta, Georgia, was called in to help examine the mutations. She and her colleagues found similar deletions and rearrangements in several other monkeypox genomes collected in the United States.

While scientists aren’t worried, they’re watching the situation closely to understand why the changes occurred and what they might mean for the global monkeypox epidemic. These mutations are a stark reminder that even smallpox viruses—which are DNA viruses that tend to evolve more slowly than RNA viruses, such as the SARS-CoV-2 coronavirus — will change over time, says Elliot Lefkowitz, a virologist at the University of Alabama at Birmingham. And the more the monkeypox virus is transmitted between humans, he adds, the more opportunities it will have to evolve.

The mutations Gigante evaluated were not the single-letter alterations scientists are used to seeing in the SARS-CoV-2 genome. In some cases, entire genes had disappeared: a section of about 7% of the genome was missing in a sample from an infected person in Florida. But it’s too early to tell whether the mutations are beneficial, neutral or harmful to the virus, Lefkowitz says. If health officials detect an increase in the number of virus samples carrying these mutations, that could be a possible signal that they are helping the virus spread.

Mutation strategies

The large deletions and rearrangements first reported in Minnesota did not surprise Eneida Hatcher, an evolutionary virologist at the National Center for Biotechnology Information in Bethesda, Maryland. In 2015, he co-authored a study with Lefkowitz that showed that such mutations are common to most smallpox viruses and that the majority of the genes they disrupt are located toward the terminal or terminal regions of the viral genome. “It was really cool to see some of the mutation strategies we’ve seen in the past play out,” says Hatcher.

Orthopoxviruses, a genus of poxviruses that includes monkeypox virus and variola virus, which causes smallpox, share a core set of about 174 genes in the center of their genomes. But their terminal regions are more variable and contain fewer essential genes. Some of the genes in these regions are thought to encode proteins that help disarm host immune responses and are tailored to infect specific hosts, Lefkowitz says. This forms the basis of one hypothesis as to why variola became capable of infecting humans: over thousands of years, an earlier version of the virus may have lost genes from its ends that allowed it to infect a wide range of animal species and eventually he became an expert in infecting people.

Some scientists worry that a similar situation could arise with monkeypox. But predicting how the behavior of the monkeypox virus will change as it mutates is difficult because researchers have yet to characterize the function of many genes in its large genome. For example, although researchers first discovered that two strains of the monkeypox virus were spreading in Africa more than 17 years ago, they are still struggling to determine exactly which genes are responsible for the difference in death rate between the two , says Lefkowitz. The mortality rate for one of them – clade I, which dominates Central Africa – is about 10%. Clade II, circulating in West Africa, has a mortality rate of about 1% to 3%.

Genome collaboration

By analyzing the monkeypox sequences, researchers are also learning more about how the virus may have sparked the global epidemic. Scientists have observed a pattern of single-letter mutations, separate from the changes first identified in Minnesota, that appear to be a genetic imprint of the ongoing battle between the human immune system and the virus. Using data collected so far to roughly estimate the number of these mutations expected each year, they estimated that the strain responsible for the global outbreak jumped from animals to humans in early 2016. That’s more than a year and a half before the strain it was detected in humans for the first time by Nigerian health officials, who declared an outbreak in their country that never completely ended.

The good news is that, although the monkeypox virus continues to evolve, no mutations have affected the part of its genome that codes for a protein that targets tecovirimat, an antiviral drug being tested for use against monkeypox in people. However, problems may eventually appear in the diagnostic tests. To detect monkeypox virus in samples, technicians perform a polymerase chain reaction (PCR) to detect target sequences in the virus genome. Gigante and her colleagues found that one of the two copies of a monkeypox target had been deleted in one of the samples they analyzed. Although the PCR test returned a positive result, the authors caution that these types of mutation could ultimately render it ineffective.

Global attention to monkeypox will help researchers understand not only the virus that causes the disease, but also smallpox viruses in general, Hatcher says. Before this year, there were only about 100 near-complete monkeypox genomes, he says. Now, about 2,000 have been deposited in established international repositories. “I’m very happy to see the international collaborative attitude towards surveillance and genomic sequencing” continued beyond the COVID-19 pandemic, she says.

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