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Study Suggests Coronavirus Disease is Mutating

While most COVID-19 mutations do not affect disease severity, some may have made it more contagious.

Severe acute respiratory syndrome coronavirus 2, the virus that causes coronavirus disease 2019 (COVID-19), is accumulating genetic mutations that may have made it more contagious, according to a study published in mBIO.

The COVID-19 pandemic has caused more than 1.19 million deaths and there have been over 46.4 million confirmed cases worldwide, according to the World Health Organization. Mutations to the virus are a combination of natural drift, which are genetic mutations that don’t help or hurt the virus, and pressure from the human immune system, according to the study.

The study included more than 5000 patients with COVID-19 in Houston, Texas. Investigators found that a mutation known as D614G, which is located in the spike protein that pries open cells for viral entry, may have made the virus more contagious.

According to the study, during the initial wave of the pandemic, 71% of novel coronaviruses identified in patients in Houston had this mutation. During the second wave of the outbreak, that number had jumped to 99.9% prevalence.

"The virus continues to mutate as it rips through the world," said study co-author Ilya Finkelstein, PhD, associate professor of molecular biosciences at The University of Texas at Austin, in the press release. "Real-time surveillance efforts like our study will ensure that global vaccines and therapeutics are always one step ahead."

A total of 285 mutations have been identified across thousands of infections, though most do not affect disease severity, according to the study. Ongoing studies are surveilling a third wave of patients to determine how the virus is adapting to neutralizing antibodies produced by the immune system.

REFERENCE:

Coronavirus mutation may have made it more contagious [News Release] October 30, 2020; Houston, TX. https://www.sciencedaily.com/releases/2020/10/201030142123.htm. Accessed November 3, 2020.

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