Back in June, Houston, Texas saw a huge surge in coronavirus cases. Scientists discovered that the strain of SARS-CoV-2 that had developed in Europe in February, and was assumed to be more contagious, had become the prevalent strain in people with the coronavirus in Houston.
Scientists from Weill Cornell Medicine, the University of Chicago, Argonne National Laboratory and the University of Texas at Austin reported their findings on a study of the Houston cases on Wednesday on the preprint server MedRxiv. The study has not been peer-reviewed.
Lead author of the study, James Musser of Houston Methodist Hospital. explains that as viruses go, oronaviruses such as SARS-CoV-2 are relatively stable because they use a “proofreading enzyme as they replicate.” But he goes on to say that every mutation is a roll of the dice.
This means that with coronavirus infection so widespread in the U.S. – there is abundant opportunity for the virus to change. We have given this virus a lot of chances,” Musser told The Washington Post. “There is a huge population size out there right now.”
A mutation on the “spike protain”
Like all coronaviruses, SARS-CoV-2 has a series of characteristic spikes surrounding its core. These spikes are what allow the virus to attach to human cells. The mutation everyone is talking about affected the spike protein and changed amino acid 614 from “D” (aspartic acid) to “G” (glycine).
The coronavirus seems to change much more slowly than other RNA viruses, probably because of the ‘proofreading’ enzyme that corrects potentially fatal copying mistakes. A typical SARS-CoV-2 virus accumulates only two single-letter mutations per month in its genome. This is about half the rate of the influenza genome.
Believe it or noy, but worldwide, researchers have sequenced over 112,000 isolates of the COVID-19 virus. Two SARS-CoV-2 viruses collected from anywhere in the world differ by an average of just 10 RNA letters out of 29,903, says Lucy Van Dorp, a computational geneticist at University College London
The virus’s genetic code has close to 30,000 nucleotides of RNA, or letters that spell out 29 different genes. And out of the over 12,000 mutations found in the SARS-CoV-2 genomes, most are of no consequence for the virus’s ability to spread or cause disease, because they do not alter the shape of a protein.
With everyone on the planet susceptible to the coronavirus, there is very little evolutionary pressure for the virus to chane much. “As far as the virus is concerned, every single person that it comes to is a good piece of meat,” says William Hanage, an epidemiologist at the Harvard T. H. Chan School of Public Health in Boston, Massachusetts. “There’s no selection to be doing it any better.”
Houston study results
What is interesting about this study is that scientists can actually see what happened when the virus first entered the Houston population in March this year. At that time, there were a number of different strains of the virus infecting people, however, by June, almost every coronavirus sample contained a particular mutation found on the virus’ surface found in Europe in February.
The study found that patients with that strain of coronavirus carried more virus particles than other people, meaning they were probably more infectious. The mutation did not make the virus more dangerous or change the outcome or course of the disease. But the number of cases did jump from about 200 new Covid-19 cases per day in Houston to more than 2,400, according to Forbes.
A similar study from earlier this month found evidence that the United Kingdom was also overtaken by the same virus strain over the spring. And like the Houston study, scientists concluded a mutation that changes the “spike protein” on the surface of the virus may be driving the outsized spread of that particular strain.
David Morens, a virologist at the National Institute of Allergy and Infectious Diseases, reviewed the new study. He noted that as the coronavirus has moved through the population – it has become more transmissible – and that this “may have implications for our ability to control it.”
While pointing out that this is just a single study, “you don’t want to over-interpret what this means.” But the virus, he said, could potentially be responding — through random mutations — to such interventions as mask-wearing and social distancing, Morens said Wednesday.
“Wearing masks, washing our hands, all those things are barriers to transmissibility, or contagion, but as the virus becomes more contagious it statistically is better at getting around those barriers,” said Morens, senior adviser to Anthony S. Fauci, the director of NIAID.
