Strictly speaking, viruses are not living organisms.
They do, however, benefit from natural selection over time. The longer a virus exists within a community the more sophisticated its pathogenesis becomes, though the articulations of this can vary. A populated gene pool helps some strains develop resistance to drug treatment. Others are rewarded quicker transmission rates. This evolution happens very quickly in RNA viruses like the one staffing our current pandemic.
According to a research paper published in Biorxiv, a new SARS-CoV-2 mutation spike called D614G has emerged and it is suspected to enable the pathogen to be more contagious than the strains previously recorded.
“We have developed an analysis pipeline to facilitate real-time mutation tracking in SARS-CoV-2, focusing initially on the Spike (S) protein because it mediates infection of human cells and is the target of most vaccine strategies and antibody-based therapeutics,” the authors wrote. “D614G is of urgent concern; it began spreading in Europe in early February, and when introduced to new regions it rapidly becomes the dominant form. Also, we present evidence of recombination between locally circulating strains, indicative of multiple strain infections. These findings have important implications for SARS-CoV-2 transmission, pathogenesis, and immune interventions.”
Spike mutation pipeline reveals the emergence of a more transmissible form of SARS-CoV-2
Before virologists were able to access SARS-CoV02’s lethal potential, they knew it spread quickly. By and large, an infected individual passes the coronavirus to three people before its incubation cycle is complete. In addition, SARS-CoV-2 fomites remain active on surfaces for days and in aerosols for hours.
A review of genetic samples taken from 7,500 patients who were exposed to the coronavirus revealed that it emerged in Wuhan around October and penetrated countries around the globe as early as December.
Since then, scientists at The University of London’s Genetics Institute determined that there are nearly 200 recurrent genetic mutations of SARS-CoV-2.
There are a lot of things that influence a virus’s evolution. A diverse community of hosts facilitates the speedy modification of a pathogen’s DNA or RNA sequencing. A random mutation occurs after more than one virus infects a person at the same time; seeing each exchange genetic material. A fair share of aggressive flu strains is actually the result of two separate strains coming together to obtain unique properties.
Only 20% of patients that develop Covid-19 succumb to it but its breakneck transmission rates have resulted in an alarmingly high mortality count.
“Three related factors combine to make this disease so dangerous: human beings have no direct immunological experience with this virus, leaving us vulnerable to infection and disease; it is highly transmissible, and it has a high mortality rate,” the authors continued. “These basic numbers, R0 and mortality, are critical for public health response planning, but are difficult to resolve with confidence or to generalize across populations, given limited diagnostic testing and variations in the strategies of estimation.”
That being said, the appearance of new coronavirus mutations isn’t actually an indication of the virus’s aggression. Many researchers anticipated multiple strains before the World Health Organization defined the coronavirus crisis like a pandemic and a similar majority remain confident that a vaccine will be made available to the public before a more destructive manifestation of SARS-CoV-2 develops.
After analyzing SARS-CoV-2 genomes, a new study published in the journal Infection, Genetics and Evolution identified 200 small genetic changes and mutations. If any of these began demonstrating a dramatic deadlier pathology in the short months since the first zoonotic strain jumped to humans, it would be highly unusual.
The response to the new mutation study from The Los Alamos National Laboratory has been mostly positive from other academicians but this has not been the case for the coverage of its findings.
Reports about the fractional changes evidenced by SARS-Cov-2 will help volcanologists develop a shortlist of targeted therapeutics but they shouldn’t be perceived as a losing battle in our war for containment. Moreover, the new report has yet to be peer-reviewed, which means its results may be repudiated in the coming weeks.
“To say that you’ve revealed the emergence of a more transmissible form of SARS-CoV-2 without ever actually testing it isn’t the type of thing that makes me feel comfortable as a scientist,” Lisa Gralinski of the University of North Carolina, said on the new research paper.
Even if the virus is categorically going through changes that will make it more deadly to hosts, there would be no evidence of it for many months to come.
Although mutations are normal, the process is a snail’s pace in the grander scheme of things-even for the quickest viral material of the bunch.
“Phylogenetic estimates support that the COVID-2 pandemic started sometime around Oct. 6, 2019, to Dec. 11, 2019, which corresponds to the time of the host jump into humans,” says the research team, co-led by Francois Balloux who co-led a research team that challenged the aggressive strain hypothesis. “All viruses naturally mutate. Mutations in themselves are not a bad thing and there is nothing to suggest SARS-CoV-2 is mutating faster or slower than expected,” he said. “So far, we cannot say whether SARS-CoV-2 is becoming more or less lethal and contagious.”
CW Headley is a reporter for the Ladders and can be reached at email@example.com