None of the SARS-CoV-2 gene mutations are shown to increase transmissibility

None of the mutations are currently documented in SARS-CoV-2 The virus appears to increase its transmissibility in humans, according to a study conducted by University College London researchers.

Analysis of the virus genomes of more than 46,000 infected people Covid-19 From 99 countries it was published today (25 November 2020) in Nature Communications.

“The number of SARS-CoV-2 genomes being produced for scientific research is staggering,” said Dr. Lucy Van Dorp (Institute of Genetics at the University of California, Lucy) and first author and interviewer, “The number of SARS-CoV-2 genomes being produced for scientific research is staggering. We realized early in the epidemic that we needed new methods to analyze massive amounts of Data in near real time to identify new mutations in the virus that could affect transmission or severity of symptoms.

“Fortunately, we found that none of these mutations cause COVID-19 to spread more quickly, but we have to remain vigilant and continue to monitor new mutations, especially as vaccines are introduced.”

Coronaviruses such as SARS-CoV-2 are a type of virus RNA The virus, which can develop mutations in three different ways: by mistake from copying errors during virus replication, or through interactions with other viruses that infect the same cell (recombination or reclassification), or can be induced by host RNA modification systems that It is part of the host’s immunity (like a person’s immune system).

Most of the mutations are neutral, while others can be either beneficial or harmful to the virus. Both neutral and beneficial mutations can become more common as they are transmitted to the lineage viruses.

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Research team from UCL, Cirad, Université de la Réunion, Oxford universityIn this article, we analyzed a global dataset of virus genomes from 46,723 people infected with COVID-19, collected through the end of July 2020.

Researchers have so far identified 12,706 mutations in SARS-CoV-2, the virus that causes COVID-19. For 398 mutations, there is strong evidence that they occurred frequently and independently. Of these, the researchers sharpened 185 mutations that occurred at least three times independently during the course of the epidemic.

To test whether mutations increase virus transmission, researchers modeled the virus’s evolution tree, and analyzed whether a particular mutation had become increasingly common within a particular branch of the evolution tree – that is, to test whether the mutation first develops in a virus, the descendants of that virus outperform SARS-CoV-2 viruses are closely related without a specific mutation.

The researchers found no evidence that any of the common mutations increase the transmissibility of the virus. Instead, they found that the most common mutations were neutral to the virus. This includes one mutation in a viral spike protein called D614G, which has been widely reported as a common mutation that may make the virus more transmissible. New evidence found that this mutation was, in fact, not associated with a significantly increased transmission.

The researchers found that most of the common mutations appear to be caused by the human immune system, rather than as a result of the virus adapting to its new human host. This situation contrasts with another analysis by the same team of what happened when SARS-CoV-2 later jumped from humans to farmed minks.

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“When we analyzed the virus’ genomes taken from mink, we were surprised to see the same mutation appearing again and again in different mink farms, despite these same mutations that were seldom observed in humans before,” said Dr. Van Dorp.

Lead author Professor Francois Ballou (Institute of Genetics at the University of California, Los Angeles) added: “We may have missed this period of early adaptation of the virus in humans. We previously estimated that SARS-CoV-2 jumped into humans in October or November 2019, but the first genomes “We have it going back to the end of December. By that time, the viral mutations critical to human transmissibility may have emerged and become invariant, preventing our study of them.”

The virus is only expected to mutate and eventually mutate into different strains as it becomes more common in humans, but this does not necessarily mean any more transmissible or harmful strains emerge.

“The virus appears to be well prepared for transmission between humans, and it may have already reached its optimum fitness in the human host by the time it has been identified as a new virus,” said Dr. Van Dorp.

The researchers warned that the imminent introduction of vaccines is likely to put new selective pressure on the virus to avoid recognition by the human immune system. This may lead to vaccine escape mutations. The team stressed that the computational framework they developed should be useful for identifying potential vaccine escape mutations in time.

Professor Ballux concluded, “The news on the vaccination front looks great. The virus may acquire escape vaccine mutations in the future, but we are confident that we will be able to report them immediately, which will allow vaccines to be updated in a timely manner if needed.”

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Reference: 25 November 2020, Nature Communications.
DOI: 10.1038 / s41467-020-19818-2

The study was supported by the NSFC Initiative of Newton Fund UK-China and the Biotechnology and Biological Sciences Research Council (BBSRC).

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