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The mutation of the coronavirus may have made it more contagious

A study of more than 5,000 patients with Covid-19 virus in Houston found that the virus that causes the disease accumulates genetic mutations, one of which may have made it more contagious. According to the paper published in the peer-reviewed journal mBIOThat mutation, called D614G, is located in the spiky protein that opens our cells to enter the virus. It is the largest peer-reviewed study of sequencing the SARS-CoV-2 genome in a single metropolitan area in the United States to date.

The paper shows that “the virus is mutating due to a combination of neutral drift – which means only random genetic changes that do not help or harm the virus – and the stress from our immune systems,” said Ilya Finkelstein, associate professor in molecular biosciences at the University of Texas at Austin and co-author. To study. The study was conducted by scientists at Houston Methodist Hospital, Utah Austin and elsewhere.

During the first wave of the pandemic, 71% of novel coronaviruses identified in patients in Houston had this mutation. When the second wave of the outbreak hit Houston over the summer, that variable jumped to a prevalence of 99.9%. This reflects a trend observed around the world. A study published in July based on more than 28,000 genome sequences found that variants carrying the D614G mutation became the globally dominant form of SARS-CoV-2 within about a month. SARS-CoV-2 is the coronavirus that causes COVID-19.

So why did strains that contain this mutation outpace strains that did not have them?

Perhaps they are more contagious. A study of more than 25,000 genome sequences in the UK found that viruses with the mutated tendency to transmit slightly faster than those without them and cause larger clusters of infections. Natural selection will delight strains of the virus that transmit more easily. But not all scientists are convinced. Some have suggested another explanation called ‘founder influences’. In this scenario, the D614G mutation may be more common in the first viruses to arrive in Europe and North America, essentially giving it a head start over other strains.

The spike protein also continues to accumulate additional, unknown mutations. The Houston Methodist-UT Austin team also showed in laboratory experiments that at least one such mutation allows the spike to evade the equivalent antibody naturally produced by humans to fight SARS infection. This could allow this type of virus to pass more easily through our immune systems. Although it is not yet clear whether this translates into more easily transmission between individuals.

The good news is that this mutation is rare and does not appear to make the disease more severe for affected patients. According to Finkelstein, the group did not see viruses that had learned to evade first-generation vaccines and therapeutic antibody formulations.

“The virus continues to mutate as it spreads around the world,” Finkelstein said. “Real-time monitoring efforts like our study will ensure that universal vaccines and treatments are always a step forward.”

Scientists observed a total of 285 mutations across thousands of infections, although most of them do not seem to have a significant effect on the severity of the disease. Ongoing studies continue to monitor the third wave of COVID-19 patients and to characterize how the virus adapts to neutralizing antibodies produced by our immune systems. Each new hit is a roll of dice, which is an additional opportunity to develop more dangerous mutations.

“This virus has given us a lot of opportunities,” lead author James Moser of the Houston Methodist told the Washington Post. “There is a huge population there now.”

Several other authors at the University of Austin contributed to the work: visiting scholar Jimmy Golihar, assistant professor in molecular biosciences Jason S. McClellan and graduate students Chia Wei Chu, Kamyap Javanmardi and Hong Chi Kuo.

The UT Austin team tested various genetic variants of the viral elevation protein, the part that allows it to infect host cells, to measure the stability of the protein, see how it binds to a receptor in host cells, and neutralize antibodies. Earlier in the year, McClellan and his team at the University of Austin, in collaboration with researchers at the National Institutes of Health, developed the first 3-D spike protein map for coronavirus for an innovation that is now entering many groundbreaking vaccine designs.

Researchers found that SARS-CoV-2 was introduced to the Houston area several times, independently, from diverse geographic regions, with virus strains from Europe, Asia, South America and elsewhere in the United States. There was widespread community outreach shortly after the COVID-19 cases were reported in Houston.

This study was supported by the Fundrain Foundation, Houston Methodist Hospital and Research Institute, the National Institutes of Health, the National Institute of Allergy and Infectious Diseases, the Welch Foundation, the National Science Foundation, and the Defense Advanced Research Projects Agency. Ilya Finkelstein is a cancer research researcher in CPRIT, funded by the Institute for Cancer Prevention and Research in Texas.

An earlier version of the paper was published last month on the medRxiv prepress server.

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