None of the mutations are currently documented in SARS-KOV-2 The virus appears to be increasing its transmissibility in humans, according to a study led by researchers at University College London.
Analysis of the genomes of viruses of over 46 000 people with COVID-19 from 99 countries is published today (25.11.2020) in Natural communications.
The first and appropriate author, Dr. Lucy van Dorp (UCL Institute of Genetics), said: “The number of SARS-KOV-2 genomes generated for scientific research is staggering. Early in the pandemic, we realized that we needed new approaches to analyze vast amounts of near-real-time data to detect new mutations in the virus that could affect its transmission or the severity of its symptoms.
“Fortunately, we have found that none of these mutations make KOVID-19 spread faster, but we need to stay vigilant and continue to monitor new mutations, especially when vaccines are expanding.”
Coronaviruses such as SARS-CoV-2 are a type of RNA a virus, which can all develop mutations in three different ways: by replication error in virus replication, through interactions with other viruses that infect the same cell (recombination or resorption), or can be caused by RNA modification systems hosts that are part of the host’s immunity (eg a person’s own immune system).
Most mutations are neutral, while others may be beneficial or harmful to the virus. Both neutral and favorable mutations can become more common when passed on to offspring.
The research team from UCL, Cirad and Université de la Réunion and University of Oxford, analyzed a global database of virus genomes of 46,723 people with COVID-19, collected by the end of July 2020.
Researchers have so far identified 12,706 SARS-KOV-2 mutations, the virus causing KOVID-19. For 398 of the mutations, there is strong evidence that they occurred continuously and independently. Of these, researchers singled out 185 mutations that occurred at least three times independently during the pandemic.
To test whether mutations increase the transmission of the virus, the researchers modeled the evolutionary tree of the virus and analyzed whether a particular mutation was becoming more common in a given branch of the evolutionary tree – testing whether, after a mutation, the offspring first developed into a virus. that virus outperforms the closely related SARS-CoV-2 viruses without that particular mutation.
Researchers have found no evidence that any of the common mutations increase the transmission of the virus. Instead, they found that the most common mutations were virus-neutral. This includes a mutation in the virus jump protein, called D614G, which is widely said to be a common mutation that can make the virus more transmissible. New evidence reveals that this mutation is not actually associated with a significant increase in transmission.
The researchers found that most common mutations appear to be caused by the human immune system, rather than the result of the virus adapting to its new human host. This situation contradicts another analysis by the same team of what happened when SARS-KOV-2 later jumped from humans into bred mink.
Dr Van Dorp said: “When we analyzed the genomes of mink-derived viruses, we were amazed to see the same mutation occurring repeatedly on different mink farms, despite the same mutations that were rarely seen in humans before.”
Lead author Professor Francois Balu (UCL Institute of Genetics) 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 we have the first genomes at the end of December. “By that time, viral mutations crucial to human transmission may have emerged and become fixed, excluding us from studying them.”
One can only expect the virus to mutate and eventually spread to different vines, as it becomes more common in the human population, but this does not necessarily mean that vines that are transmissible or harmful will emerge.
Dr van Dorp said: “The virus appears to be well adapted for human transmission and may have already reached its optimal fitness in the human host by the time it was identified as a new virus.”
Researchers warn that the inevitable introduction of vaccines is likely to put new selective pressures on the virus to avoid recognition by the human immune system. This can lead to the appearance of mutants to escape the vaccine. The team stressed that the computational framework they have developed should prove useful for the timely identification of possible mutations to escape vaccines.
Professor Balu concluded: “The news on the vaccine front looks great. “The virus could well acquire mutations to escape vaccines in the future, but we are confident that we will be able to label them immediately, allowing for timely vaccine updates if needed.”
Reference: November 25, 2020, Natural communications.
DOI: 10.1038 / s41467-020-19818-2
The study was supported by the NSFC initiative of the Fund Fund of Great Britain and China and the Biotechnology and Biological Sciences Research Council (BBSRC).