Researchers at the University of Texas at Austin report that mutations may have made the coronavirus more contagious. As SARS-COV-2 evolved, the D614G mutation located in its spike protein made the virus more infectious, allowing it to spread more easily.
The study involved more than 5,000 COVID-19 patients in Houston, and was focused on the various genetic mutations emerging in different strains of SARS-COV-2 since the time of the initial outbreak.
According to the researchers, the spike protein is continuing to accumulate additional mutations with unknown abilities. Lab experiments revealed that at least one such mutation allows the protein to evade a neutralizing antibody that humans naturally produce to fight SARS-CoV-2 infections.
“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 study co-author Professor Ilya Finkelstein.
In collaboration with experts at Houston Methodist Hospital, the UT Austin team tested different genetic variants of the spike protein, which is used by the virus to gain entry into host cells. The experts measured the protein’s stability by examining how well it binds to a receptor on host cells and to neutralizing antibodies.
The researchers found that SARS-CoV-2 was independently introduced to the Houston area many times from diverse geographic regions, including virus strains from Europe, Asia, South America, and elsewhere in the United States.
During the initial wave, 71 percent of the coronaviruses identified in COVID-19 patients in Houston had the D614G mutation on the spike protein. When the second wave of the pandemic hit Houston during the summer, this variant was found in 99.9 percent of the patients.
The same trend has been observed worldwide. A study that was based on more than 28,000 genome sequences showed that SARS-COV-2 strains with the infectious mutation took over as the globally dominant form of SARS-CoV-2 in about one month.
In another study of more than 25,000 genome sequences in the U.K., experts have determined that the D614G mutation allowed viruses to transmit faster than those without it and caused larger clusters of infections.
Some scientists believe the D614G mutation may have simply been more common in the first viruses to arrive in Europe and North America, which would have given them a head start on other strains.
“The virus continues to mutate as it rips through the world,” said Professor Finkelstein. “Real-time surveillance efforts like our study will ensure that global vaccines and therapeutics are always one step ahead.”
Overall, the team found a total of 285 mutations across thousands of infections, most of which did not seem to affect the severity of COVID-19. Ongoing studies will continue to monitor the third wave of COVID-19 patients to understand how the virus is adapting to neutralizing antibodies that are produced by our immune systems. Each new infection gives SARS-CoV-2 an additional chance to develop more dangerous mutations.
“We have given this virus a lot of chances,” study lead author James Musser told The Washington Post. “There is a huge population size out there right now.”
The research represents the largest peer-reviewed study of SARS-CoV-2 genome sequences in one metropolitan region of the United States.
The study is published in the journal mBio.