The coronavirus is highly contagious, that fact has been made clear by now. It sets it apart from other viruses, other flu-like epidemics, because of the intensity of its contagious nature. So, the last thing we want to read about is a strain of the virus that seems to have mutated to a more contagious one. Yet, here we are.

Let me say right up front that this is a report, an analysis by Houston Methodist Hospital, using the coronavirus circulating in the Houston area. It is an analysis of the genetic makeup of the first infections treated here. And, it is just now beginning to be peer-reviewed. So, there are no concrete conclusions available yet. That’s been the problem with this virus, though, hasn’t it? It’s been hard for medical professionals to get a firm grip on symptoms, diagnoses, and treatment options.

Beginning in early March, the virus that causes COVID-19 was introduced to the Houston area. It was first diagnosed in patients who were returning from a cruise, a group of teachers who became infected during a Nile River cruise. The earliest diagnosis was reported on March 5. That outbreak was likely caused by an Asian or European strain. To date, there have been no strains associated with Africa. Dr. James Musser, chairman of pathology and genomic medicine at Houston Methodist and a study author, says they have a snapshot of what the virus looked like after arriving in Houston. This snapshot allows scientists to keep an eye out for less severe or more severe strains of the virus. It is likely the seedling of the coronavirus came from Asia, Europe, or South America – a multiple of geographic regions. Musser attributes international origins of the outbreak in Houston to the city being “an ethnically diverse, international city and transportation hub.”

The study found no evidence yet of mutations making any particular strain of the virus more virulent than others.

But 70 percent of the specimens studied, taken from COVID-19 patients treated at Methodist between early March and March 30, had a mutation that changes the structure of a protein critical to the virus’s ability to infect human cells. Researchers at Los Alamos National Laboratory reported a week ago that the structural change enhances infectivity.

The Methodist study analyzed samples of the virus from the first 320 patients diagnosed and treated at the system’s eight hospitals. This number represents 40% of all confirmed cases in the area at the time. This percentage of cases is likely due to the hospital having its own molecular diagnostic test at a time when testing was very limited.

The test allows Methodist researchers to sequence all the genetic material in a virus — its genome. Genomes from a number of virus samples allow them to compare mutations.

The team tested the hypothesis that distinct viral groups were associated with disease severity but found little evidence to support the idea. But Musser said the matter warrants further study with a larger sample size and that such analysis is currently under way at Methodist.

The study also found no resistance-related mutations to antiviral drugs such as Remdesivir, recently approved by the Food and Drug Administration as an emergency COVID-19 treatment. The strains studied likely would respond well to Remdesivir, according to the study.

So, while the early, limited results are encouraging, the larger sample size study that is ongoing should provide more clarity. Obviously, 320 viral samples out of 1.3 million people who have been infected globally is a very small sample of the pandemic. Methodist Hospital continues to do genomic analyses of every one of its COVID-19 patients, which now number more than 1,000 cases sequenced. Musser is working on a manuscript of those cases. Knowing where the virus strains originated is important in following spikes of outbreaks, new outbreaks, and making strategies moving forward.

The Methodist study is the third such genomic analysis of the virus’ spread in a U.S. community and the largest to date. The others were in Seattle and New York City. Methodist Hospital’s paper has been submitted for peer review to a prominent scientific journal.

There is skepticism in the scientific community about the virus mutating. Many scientists do not believe that there are two strains of the coronavirus.

A study by Los Alamos National Laboratory, cited by the Los Angeles Times, found a mutation in COVID-19, known as D614G, that changes the protein’s shape. The mutated form of COVID-19 became predominant in Europe, Australia, and North America. But many scientists agree there isn’t enough evidence in the Los Alamos study to prove the mutation resulted in a different strain of COVID-19.

Though COVID-19 has developed mutations, it is unlikely it has changed enough to be considered a new strain. Viruses “copy” themselves when they spread and commonly form mutations. Mutations are random and neither good nor bad.

Mutating into a different strain, however, means the virus has changed so much it no longer “acts” like the original virus. Different strains of the same disease often respond differently to vaccines. This is why it is important to find when the virus forms a new strain.

Though researchers at Los Alamos posited the D614G mutation could have helped COVID-19 spread faster and further, researchers at Arizona State University came to the opposite conclusion in a separate study. So for now, scientists generally agree there is only one strain of COVID-19, and mutations have not yet made the virus more contagious, dangerous, or resistant to treatment.

Of the scientists who support the analysis that there are two strains of the coronavirus, with one more aggressive than the other, all agree that in order to make an effective vaccine all strains must be identified. A vaccine will have to target features in all strains of the virus. Studies involving larger groups of cases will be necessary.