The novel coronavirus, more accurately referred to as SARS-CoV-2, is an RNA virus: a mass of genetic material stored inside protein cells.
Like the documented coronaviruses that preceded it, SARS-CoV-2 is gradually mutating.
RNA viruses are much more prone to change compared to DNA viruses, even if these changes are mostly subtle in the broad scheme of things.
Since March, reports of significant coronavirus mutations have been inconsistent. When these kinds of developments made news it was typically by reason of transmissibility concerns.
Following in this tradition arrives a new study published in the medRxiv journal. In it, the authors provide evidence that the novel coronavirus may have mutated into a more contagious incarnation. Presently, there is no evidence that indicates these mutations cause a more severe form of COVID-19.
It should be noted that although the following finds have yet to be peer-reviewed, it’s data is supported by two studies previously covered by Ladders.
“We sequenced the genomes of 5,085 SARS-CoV-2 strains causing two COVID-19 disease waves in metropolitan Houston, Texas, an ethnically diverse region with seven million residents,” the authors wrote in the new paper. “The genomes were from viruses recovered in the earliest recognized phase of the pandemic in Houston, and an ongoing massive second wave of infections. The virus was originally introduced into Houston many times independently.”
Massive second wave of the SARS-CoV-2 virus and RNA mutation
The researchers involved in the medRvix report observed two different COVID-19 waves in Houston between spring and summer.
When virologists collected RNA samples toward the end of July, mutations previously documented in Europe appeared to be staffing outbreaks all across Texas. Carriers infected with these new genetic sequences shed more viral debris than those infected with the initial strains.
According to the authors, this mutation caused the region’s average transmission rate to increase from around 200 new COVID-19 cases per day to over 2,400.
This development case-hardens the race toward an effective vaccine ahead of winter.
“Our study is the first analysis of the molecular architecture of SARS-CoV-2 in two infection waves in a major metropolitan region,” the authors continued. “The findings will help us to understand the origin, composition, and trajectory of future infection waves, and the potential effect of the host immune response and therapeutic maneuvers on SARS-CoV-2 evolution.”
The impressive rate at which SAR-CoV-2 is able to adapt is actually due to a genetic shortcoming.
When DNA viruses replicate their genetic material, they do so by mimicking the host cells they infect. This process ensures errors occur less frequently than they do with RNA viruses.
RNA viruses replicate their own material in a more unique fashion– allowing deviations to occur. The very same deviations keep sophisticated pathogens a few steps ahead of natural and clinical immunity.
The best way to subvert this process is by limiting the novel coronavirus’ exposure to cells to infect. This will allow medical professionals to gain ground with respect to counter -pharmaceuticals.
“We’ll have to chase the virus and, as it mutates, we’ll have to tinker with our vaccine,” David Morens, a virologist and advisor at the National Institute of Allergy and Infectious Diseases, said of the new study.