A new study prompted scary headlines this week about a mutation in the novel coronavirus that could possibly make it more contagious.
The paper from scientists at Los Alamos National Laboratory in New Mexico and researchers in the U.K. warns of a mutation affecting the “spikes” on the SARS-CoV-2 virus. This new strain has become more prevalent, the authors say, meaning it could theoretically make the disease spread faster and more people ill. They call it an “urgent concern.”
Almost immediately, debates began over the data and what exactly it revealed. The Los Angeles Times published a story with the title, “Scientists say a now-dominant strain of the coronavirus could be more contagious than original.” The New York Times reported that a “turbocharged” version of the coronavirus was unlikely. Experts have been mixed about what the results of the study could mean, wondering if there might be other reasons we’re seeing a more dominant strain of the virus crop up in recent months.
So, what’s the deal? Is a new strain of the virus actually capable of spreading wider and faster, and should we be concerned?
The study reveals there’s a new dominant strain of the virus, but it’s not necessarily a more infectious one. If you look at SARS-CoV-2 under a microscope, you can see tiny “spikes” on the virus, which are what it uses to attach to your cells and make you sick. The study found that these spikes are actually mutating, explained Kirsten Hokeness, chair of the department of science and technology at Bryant University and an expert in immunology, virology and microbiology.
“The crown-like spike proteins are what the virus uses to infect host cells so that it can replicate and then exit,” said Hokeness, who was not affiliated with the study. “So, the spike plays an important role in the life cycle of the virus in humans. Without it, we would not get infected.”
Frank Esper, a pediatric infectious disease specialist at the Cleveland Clinic Children’s Hospital who was also not affiliated with the study, said the paper (which has not yet been peer-reviewed) indicates a spike-protein mutation called D614G has become more prevalent since the virus originated in China.
Comparing the early version of the virus found in China to those in Europe and elsewhere, the researchers found this newer mutation of the virus has seemingly become the more dominant strain. It’s now more common.
A mutation, especially in the spike part of the virus, can arguably make the virus better able to perform its primary function ― replicate and infect. But it’s not clear that this new, dominant strain of the virus will become more contagious or superpowered.
This strain may be more “fit” or “stable,” Esper said, meaning it is less likely to mutate as quickly as the initial strain. That doesn’t necessarily mean it’s more contagious.
Both experts appreciate the paper’s findings about the mutation, but think the study might go too far in its claims. For instance, it could be that the virus had more opportunity to spread in certain places before governments forced citizens into lockdown, which is why the mutation is more prevalent.
Is it possible that the new strain is more transmissible? Maybe. But we don’t know that yet, and that doesn’t necessarily make it more infectious than it already is.
“There is no evidence in the literature that suggests that this mutant strain would be or could be worse by increasing the infection rate, hospitalization or even deaths,” Hokeness said. “I would argue that this is not something of ‘urgent’ concern as the authors suggest, but it is something that warrants further investigation.”
The fact that the novel coronavirus mutated into a new strain isn’t something groundbreaking, either. Any virus can “replicate very quickly and in massive amounts,” Hokeness said, so finding new genetic sequences is not strange.
“Each cell that [the virus] infects can make upwards of a million copies of the virus,” she said. “This rapid rate of replication is very prone to errors,” which can add up quickly. Errors then get passed on to new viruses, that then replicate again, resulting in minor mutations from the original form.
In fact, in the case of this recently identified SARS-CoV-2 strain, you might even think of it as “a new lineage of a virus,” rather than a completely new, different strain, because it is such a small change overall, Hokeness said.
“If you think about viruses, they must find a host to survive, and like a vigorous cancer, they will do what they must to stay ‘alive.’ When the virus initially jumped from bats to humans, as we think it did, it was able to unlock the human receptors and gain access to the cell to multiply,” she said.
Hokeness said it’s likely the novel coronavirus “perfected” its jumping capability “as it spread through the human population, meaning that the virus could have changed its structure to more easily infect people.” It might simply be a more efficient strain, not one that creates different or more severe symptoms.
She likened the virus’s mutation process to getting a key made for your front door ― it unlocks the door but may be a little hard to get in and out of the lock.
“If you shave the key just a bit it can now easily fit into the lock without trouble,” she said. Finding “small ways to access the receptor just a bit better,” can make some strains more likely to persist.
And despite some change, the novel coronavirus still appears to be a little more stable, or less prone to mutation, than other RNA viruses due to its size, Esper said. (RNA is a type of genetic material contained in the virus; SARS, the flu and Ebola are also considered RNA viruses.)
“This virus is one of the biggest RNA viruses out there,” he said. “Because it is large, it actually has a good polymerase, which is the enzyme that allows it to replicate.” This means the virus can “proofread” its genetic sequence better than smaller viruses like HIV and the flu.
“This virus is checking, making sure what it wrote is what it wants to write, so there are fewer mistakes,” he said. “Therefore its mutation rate is a lot lower. Mutating is an evolutionary advantage. It’s why the flu comes every year, and HIV is so tough to eradicate.”
But right now, the novel coronavirus doesn’t really need to mutate very much. “It is a strong virus,” Hokeness said. “It has transmissibility that is remarkable in many ways, like the levels of asymptomatic spread, which means we most likely won’t see major changes any time soon.”
She said mutating is a situation where if it isn’t broken, why fix it? “This virus is good at what it does, so there is not a lot of evolutionary pressure for it to mutate,” Hokeness said. “Any mutations that make it less effective would be accidental and a result of mistakes in replication.”
If the virus is more stable and mutates less, it may lead to a better vaccine or treatments
Researchers need to monitor changes to the coronavirus spikes for a simple reason, which is why this recent study is still important, even if the conclusion might be a little overblown. Targeting the spikes is likely how researchers are going arrive at a treatment, because it’s how the virus attaches to cells in the body.
It is important to understand the stability of the virus, how much or how little the virus changes over time, “particularly as we work to find treatments such as a vaccine” and “further unravel degrees to which the population can develop immunity to the virus,” Hokeness said.
“If you look at most of the vaccines that are in clinical trials right now, they are targeting that spike protein these authors are looking at,” Hokeness said. “If the spike proteins mutate to a large degree, any vaccine that targets that will not work or won’t work well.”
On top of that, mutations can affect natural immunity. “If a virus mutates in a way that the immune system can’t recognize it, it would mean that even people who got the virus during this first infectious cycle, could get it again, as the immune system wouldn’t recognize it,” Hokeness said.
For these reasons, the stability we’re seeing in the virus right now is a good thing, because there will be a better chance of winding up with an effective vaccine (eventually).
“I do not expect it to behave like the flu,” Esper said. “It comes down to the proofreading function. Flu changes so much; it basically reinvents itself each year, so much so that we need a new vaccine.” Because the novel coronavirus has such an effective polymerase enzyme ― the proofreading system to keep it from making errors ― it’s unlikely to mutate as much or as fast, Esper said.
He speculated that it is “still going to be a pretty similar virus a year from now.”
Currently, there are not a lot of respiratory viruses for which we have vaccines, said Esper.
“One is flu and the other is measles,” he explained, noting the huge difference between the two. With the flu, you need a new shot every year. “But the measles works great; you only get two in a lifetime,” he said. “We can make very good vaccines against respiratory viruses. All our vaccines have to be safe. But when we find one, I think it will be good.” #KhabarLive #hydnews