The virus that produces COVID-19 is mutating — really quick. Here’s what that implies for your danger of infection and symptoms.
The immediate explanation is a lot, but only one strain is involving doctors at this time: The scientific society has been whirring with the disturbing news that the virus that produces COVID-19 may have mutated in such a form to make it more contagious. A preparatory study from April 30 and different on June 12 recommended that the virus variant, called G614, hides a feature that allows the virus to more quickly infect cells and consequently spread more swiftly. The anxiety grew even more last week when Anthony Fauci, MD, head of the National Institute of Allergy and Infectious Diseases (NIAID), opened the idea through an online chat.
A mutation that increases the rate of COVID-19’s infection might reveal why the virus—known as SARS-CoV-2—has so quickly passed through North America and Europe, where the G614 mutated version is surpassing. The initial version of the virus, D614, was most extensively seen in China and other parts of Asia.
How concerned should we be?
Not all specialists are satisfied the virus has mutated into a more transmissible form. “I do not feel that we have concrete data that lead us to confidently say that,” says Greg Poland, MD, an expert with the Infectious Diseases Society of America (IDSA). A report posted on July 3, 2020, in the journal Cell claims that the contagious nature and other characters of the active virus’s characteristics are still unclear.
What is the consequence of a virus that may have mutated to spread more effectively, and how would that influence attempts to curb the pandemic?
How frequently do viruses transform?
There are two types of viruses currently worldwide: DNA viruses, which contain two same strands of genetic data, and RNA viruses that have just one strand. Like influenza, SARS-CoV-2 is an RNA virus. “All RNA viruses mutate. It’s not possible for them not to mutate,” says Dr Poland, who is likewise a director of the Mayo Vaccine Research Group in Rochester, Minnesota, and editor-in-chief of the journal Vaccine.
“Mutations mean genetic changes in the virus. Those mutations can make the virus less severe, more severe, or no change.”
Not only do RNA viruses mutate, but they also mutate almost instantly. DNA viruses have two strands of genetic information, so a mutation on one strand can soon be detected and deleted.
With only one strand of genetic information, RNA has no inherent fact-checking mechanism, and mutations linger and reproduce.
Increased infections mean increased mutations.
As viruses progress through humans, the more they can reproduce and the more possibilities they will be able to mutate. SARS-CoV-2 mutates less quickly than the influenza virus but, by now, has passed through numerous hosts and replicated so many times, there are hundreds, thousands, or even more mutations out there, says Dr Poland. The enormous majority of these, he adds, are hereditary failures and will fall by the wayside.
But there will only be more extensive mutations. “Due to the lack of proofreading, SARS-CoV-2 should continue to mutate at the present rate,” explains S. Wesley Long, MD, Ph.D., assistant professor of pathology and genomic medicine, Houston Methodist Hospital, also adding that “most of these mutations have no effect on the virus.”
What’s distinctive about the G614 mutation?
The G614 mutation is a shift in one amino acid – It is more specifically the one that has captured everyone’s attention. It changes the spike (S) protein, the one that juts out from the exterior of the virus similar to a spoke on the Statue of Liberty crown.
This spike enables the virus to enter inadvertent host cells. The new research implies that the spike protein carrying that mutation might be more thriving at infecting cells, says Dr Long. Once in the cell, the virus has more opportunities to reproduce and mutate.
None of the analysis thus far has shown that the mutated virus may cause more severe illness.
“It’s important to remember that COVID-19 with this mutation has been common in the United States and Europe since March, and there is absolutely no evidence that this mutation or any other mutation makes a particular strain of COVID-19 more severe or more deadly,” adds Dr Long.
Does the mutation reveal transmission movements?
Admittedly, becoming different strains of the virus could demonstrate regional variations in how the fast it spreads, but experts are far from being able to state that. Yet different preparatory research paper updated on June 30 concludes that G614 does not increase transmissibility.
More often, says Dr Poland, enhanced transmissibility is due to genetic factors in the host, and there is no deficiency of those. “It could be cultural reasons, access to care, more diabetes, more obesity, less compliance, on and on and on,” says Dr Poland.
Will these affect the vaccines and medications?
Mutations can affect the inherent effectiveness of vaccines and treatments. One of the reasons we’ve had such difficulty formulating a vaccine for HIV is that the virus mutates so rapidly. Says Dr Poland, it mutates amid treatment, rendering a treatment completely useless. That’s why people need to take various drugs at one time to outwit the virus, he adds.
For now, the SARS-CoV-2 mutations don’t affect medications or vaccines, primarily because both are still in development. “Mutations could occur which might affect potential vaccines or the effectiveness of antiviral therapies,” says Dr Long. “This is one reason the flu vaccine changes annually. Thus far, with SARS-CoV-2, no such mutations have been identified, but treatments and vaccines are also in development, so it is difficult to predict the unknown.”
Is there a light at the end of this tunnel?
A preliminary study of SARS-CoV-2 genes progressions from patients co-written by Dr Long found no evidence of mutations that would make the virus resistant to antiviral drugs like remdesivir, which has been revealed to promote recovery rate in adults with COVID-19. Quite the opposite, the SARS-CoV-2 strains they looked at resembled to respond well to remdesivir.
It’s not out of the issue that SARS-CoV-2 could emerge into a virus similar to influenza, which has repeated waves or seasonality; nevertheless, says Dr Poland, “that’s a remote possibility.”
Prevention will always be better than Cure.
So that takes us back to the one thing we do know about: Limiting COVID-19 infections.
“There are only two ways to get infected with the virus,” says Dr Poland. The first way is to breathe it in. The second way is to touch a contaminated surface and then touch your eyes, nose, or mouth.
Support social distance, stay away from crowded places, wear a mask, and wash your hands regularly with soap and water if they’re accessible. If not, use an alcohol-based hand sanitizer.
“There’s nothing mysterious or mystical or evil about this,” he adds. “If you wear a mask, if you keep your hands clean, and if maintain social distancing, you can’t get infected.”
This post was originally published on The Healthy.
- bioRxiv Preprint: “Spike mutation pipeline reveals the emergence of a more transmissible form of SARS-CoV-2.”
- bioRxiv Preprint: “The D614G mutation in the SARS-CoV-2 spike protein reduces S1 shedding and increases infectivity.”
- YouTube: “Conversations with Dr. Bauchner.”
- Greg Poland, MD, IDSA expert, professor of medicine and infectious disease, Mayo Clinic, Rochester, Minnesota, director, Mayo Vaccine Research Group and editor-in-chief, Vaccine.
- Cell: “Making sense of mutation: what D614G means for the COVID-19 pandemic remains unclear.”
- S. Wesley Long, MD, PhD, assistant professor of pathology and genomic medicine, Houston Methodist Hospital.
- bioRxiv Preprint: “No evidence for increased transmissibility from recurrent mutations in SARS-CoV-2.”
- bioRxiv PrePrint: “Molecular Architecture of Early Dissemination and Evolution of the SARS-CoV-2 Virus in Metropolitan Houston, Texas.”
- New England Journal of Medicine: “Remdesivir for the Treatment of Covid-19 — Preliminary Report.”