Coronavirus mutation may have made it more contagious

October 30, 2020

A study involving more than 5,000 COVID-19 patients in Houston finds that the virus that causes the disease is accumulating genetic mutations, one of which may have made it more contagious. According to the paper mBIO, that mutation, called D614G, is located in the spike protein that pries open our cells for viral entry. It's the largest peer-reviewed study of SARS-CoV-2 genome sequences in one metropolitan region of the U.S. to date.

The paper shows "the virus is mutating due to a combination of neutral drift -- which just means random genetic changes that don't help or hurt the virus -- and pressure from our immune systems," said Ilya Finkelstein, associate professor of molecular biosciences at The University of Texas at Austin and co-author of the study. The study was carried out by scientists at Houston Methodist Hospital, UT Austin and elsewhere.

During the initial wave of the pandemic, 71% of the novel coronaviruses identified in patients in Houston had this mutation. When the second wave of the outbreak hit Houston during the summer, this variant had leaped to 99.9% prevalence. This mirrors a trend observed around the world. A study published in July based on more than 28,000 genome sequences found that variants carrying

So why did strains containing this mutation outcompete those that didn't have it?

Perhaps they're more contagious. A

The spike protein is also continuing to accumulate additional mutations of unknown significance. The Houston Methodist-UT Austin team also showed in lab experiments that at least one such mutation allows spike to evade a neutralizing antibody that humans naturally produce to fight SARS-CoV-2 infections. This may allow that variant of the virus to more easily slip past our immune systems. Although it is not clear yet whether that translates into it also being more easily transmitted between individuals.

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

"The virus continues to mutate as it rips through the world," Finkelstein said. "Real-time surveillance efforts like our study will ensure that global vaccines and therapeutics are always one step ahead."

The scientists noted a total of 285 mutations across thousands of infections, although most don't appear to have a significant effect on how severe the disease is. Ongoing studies are continuing to surveil the third wave of COVID-19 patients and to characterize how the virus is adapting to neutralizing antibodies that are produced by our immune systems. Each new infection is a roll of the dice, an additional chance to develop more dangerous mutations.

"We have given this virus a lot of chances," lead author James Musser of Houston Methodist told

Several other UT Austin authors contributed to the work: visiting scholar Jimmy Gollihar, associate professor of molecular biosciences Jason S. McLellan and graduate students Chia-Wei Chou, Kamyab Javanmardi and Hung-Che Kuo.

The UT Austin team tested different genetic variants of the virus's

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

This study was supported by the Fondren 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 CPRIT scholar in cancer research, funded by the Cancer Prevention and Research Institute of Texas.

An earlier version of the paper was posted last month to the preprint server medRxiv.
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University of Texas at Austin

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