News of an emerging new strain of the novel coronavirus has led to many questions and concerns. First detected in England about a month ago, it has quickly appeared in over 20 countries and, last week, several cases were already discovered in the U.S. — where, likely, it has already been circulating for some time.
Scientists have suggested that the new strain, while apparently not more lethal, can spread significantly faster, with some suggesting that it could be up to 70% more transmittable than earlier strains. The outbreak comes as Great Britain, America, and much of the world see a surge in cases and hospitalizations, raising the specter of tighter restrictions on commerce and daily life to reign the pandemic in.
The new strain’s emergence has also raised concerns that significant mutations could potentially undermine the effectiveness of the newly released vaccines just starting to reach the population.
In an effort to address some of these matters, Hamodia spoke with Dr. William A. Petri Jr., M.D., Ph.D., a chaired professor of infectious diseases and international health at the University of Virginia and vice chair for research in its Department of Medicine. He is currently studying the effects of COVID on the immune system, and researching both treatment and vaccines to address the virus.
Below is the exchange, which has been edited for clarity and brevity.
What led scientists to believe that the new strain that emerged in the U.K. is more contagious than those presently circulating?
I think the clearest evidence is that right now the majority of cases in the U.K. are from this variant. In London it accounts for 60% of the cases. It’s an easy thing to pick up because this mutation generally comes up negative for one of the three amplification targets that the PCR tests base their diagnosis on.
They first took notice of this strain in Kent, England, in early December, when they saw a surge of cases there and then noticed that 50% were by this one variant, which itself has 17 mutations.
It is logical that a more transmittable variant of the virus will have a reproductive advantage and when you have millions of people being infected, even a small relative advantage like transmission is going to out compete the less transmittable ones.
Neither of these points prove that it’s more contagious, but they certainly are serious causes to be concerned that it is.
There are other feasible explanations. It could be that there was a bottleneck of people with this strain and it got transmitted from one person to another and ended up spreading by chance, but that it is not necessarily more contagious. I think that as it begins to spread around the U.S., we will find out in a few weeks how much of a difference these mutations really make.
Assuming that this strain is more contagious, is there a way to explain in layman’s terms what causes that to be the case? Is it something in the makeup of the virus itself or does it transfer more easily between people by staying airborne longer; or something along those lines?
No one really knows why right now. The suspicion is that there is something about the spike proteins that we are used to seeing in magnified pictures of the virus that allow them to bind to receptors and get into the cells more easily, thereby causing infection. If that would be the case, it would be a logical reason for it to be more transmittable. We know that one of the mutations in this new strain does allow the virus to bind tighter to human cells, which could explain why it is more easily transmitted from person to person.
But, it is also possible that there is something about these mutations that allows them to become more aerosolized and to remain more stable in the environment for a longer time than other variants, allowing them to spread more easily.
How quickly is it likely for this strain to become widespread in America as well?
It really depends on whether in fact it is more transmissible. Then we would expect to see the same thing happen in the U.S. that has happened in the U.K., that this will become the predominant variant.
Is the pace at which this variant appeared, that is, the rate at which COVID-19 is mutating in general, common to viruses of this sort? Is it moving slower or faster than other comparable viruses?
In a general sense it’s mutating slower than other comparable viruses. If you look at influenza or seasonal coronaviruses that cause common colds, they mutate much more frequently and significantly.
The virus is unique among RNA viruses in that it has something akin to a built-in proofreader. Just like Microsoft Word has an automatic spellcheck, this coronavirus has a proofreader that corrects mistakes, which makes its RNA more genetically stable than other viruses. The silver lining of that is that once a person has some level of immunity, it makes the virus a stable target for the immune system to fight off.
Even with the proofreading correcting variations, though, with millions of people infected, you will see new variants arise due to the sheer amount of virus that is out there. The additional piece of the puzzle is that, with so many people infected, you will have a certain amount of immune-deficient people in the mix as well. When they get infected, since they have a harder time fighting the virus off, it can stay in their body for a longer period of time than is typical and that gives the virus a safe place to mutate. Consequently, those people can then pass along that mutated version to others.
Many viruses become less potent when they mutate. Could these changes be the beginning of COVID becoming a less dangerous virus?
It’s reasonable to expect that to happen at some point, the question is the rate at which it will occur.
If you think about it, it’s not in the virus’ best interests to kill people, because when it does that it hits a dead end. What it really wants, so to speak, is to be very transmittable but not so lethal. That’s the evolutionary direction that a virus should be expected to take.
But what we don’t know is whether that will take months or years to actually happen and the downside of COVID having the RNA proofreader that I mentioned is that it could likely make that process go significantly slower.
Until now, reinfection is a phenomenon that is possible, but very rare. Is it likely that the emergence of this new strain or other mutations could make it more common?
It’s possible that it will and that is something that is being tested right now to see how much convalescent plasma from recovered COVID patients or serum from vaccine developed antibodies neutralizes this new strain. There was one preprinted study this week which showed slightly less neutralization of the new variant, but that is a very preliminary result, and it would be unexpected for that to be true.
We’ve already seen dozens of variants or genetic mutations, but all of them have been neutralized by the antibodies produced by vaccine responses. The reason for that is that there are multiple sites on the virus’ spikes that an antibody can bind to and neutralize. So, it has multiple ways to attack it. That said, what is concerning about this new variant is that it has eight mutations in the spikes, not just a single one like most previous mutations. That could pose more of a challenge to antibodies. Still when we talk about immunity, antibodies are not the only factor, because cellular immunity could also be helpful.
I think these are questions that we are going to know much more about in a few weeks. It’s not 100% sure, but based on what we know it seems likely that the existing immune responses will hold up against this variant.
Is it accurate to say that the same thinking is why the present vaccines are thought to be equally effective against this new strain?
Yes. This is not the first variant of the virus and with the dozen or so older variants that the vaccines were tested on, they were all neutralized by the antibodies the vaccines produce, so there is no a priori reason to think that this one is going to be different. The only possibility that this could be an exception is because of the eight mutations in the spikes which is why it does need to be tested.
Even if vaccines prove effective against this variant, are you concerned, should mutations continue, that it could reach a point that they would cease to be effective?
That is a possibility, but one factor that argues against that happening is that the virus only has so much leeway to make mutations since the spike glycoprotein has to be able to bind to two human proteins (ACE2 and neuropilin) in order to get into cells and infect people. That limits how much it can mutate away from the original script and still be able to transmit. In a way, the spike, like a protein, is the Achilles heel of the virus because it limits its ability to mutate and adapt.
The beauty of the RNA vaccines that are in use now is that in the worst-case scenario that they do not adequately neutralize new variants, they can very quickly just swap out that RNA and put in a new one that reflects the mutations of new variants. That’s something that would work if they are not as effective as we think they are against this variant and, if necessary, it could be done for variants down the road. So even that worst-case scenario can be pretty easily addressed.
Right now, there are plans to keep on vaccinating the population as the year goes on. If scientists would have to make the changes you mentioned in order for vaccines to remain effective, how much would that slow the process down?
We’re talking about something that hasn’t happened, and that’s unlikely to happen.
But in the unlikely event that mutations will be able to escape the vaccines, then the beauty of these vaccines is that they’ve already been proven to be safe and effective. That is the most time-consuming part of the process and it’s already been done.
All that would remain would be a very simple process to change the internal RNA codes. So, we’re probably talking about doing a study with around 1,000 individuals with a modified vaccine that gets the new variant, not 60,000 people that it would take to show safety and effectiveness. So, it would be a much faster, simpler process than the original development.
Does the emergence of this strain put more pressure on public health planners to roll out vaccination faster?
Well, one other piece of these questions is that if this variant is indeed more transmissible, we will need a higher percentage of people to be immunized in order to achieve herd immunity.
If one infected person infects an average of three other people, then estimates are that we would need 60%-70% immunity to arrive at herd immunity.
But if this changes that equation and makes it such that one infected person infects an average of four to five other people, then we would likely need upwards of 90% to get to that herd immunity level. It is an important point to consider. Even if it would not require any change in vaccine itself, there would need to be very aggressive and coordinated distribution and a strong emphasis on explaining to people how crucial vaccinations are to protecting themselves, their families and the population at large.
What is your outlook for how the emergence of this strain will affect the future of efforts to combat the pandemic?
This new strain out of the U.K. is not the only potentially significant development in viral mutations.
There’s also a new variant in South Africa that shares this one mutation in the spike glycoprotein that increases the ability of the virus to bind to the human receptors.
That supports the idea that these changes may be affecting transmissibility and it’s one of several factors that needs to be tested.
Both developments underscore the importance of following the genetic evolution of the virus as this pandemic continues.
Even though the virus has this proofreader element, it’s under tremendous pressure, so to speak, to be more transmissible and, hopefully, less virulent.
This is going to be a continued theme throughout the pandemic; as the virus continues to change, we’ll need to do what we can to understand the importance of those changes.