With the U.S. on Tuesday recording its first known case of the novel coronavirus variant that’s been sweeping across the U.K., the pressure is on to track the variant’s spread and parse out why it seems to be more contagious – and what that means for the future of the pandemic.

At the center of those efforts is a group at the Seattle-based Fred Hutchinson Cancer Research Center that has been cataloging and analyzing genetic changes in the virus since the pandemic began. Nextstrain, co-founded by Hutch computational biologist Trevor Bedford, is an uber-dashboard of genomics, mapping out mutations and the routes followed by every known variation of the virus so far.

Now, Bedford and the project’s far-flung team of bioinformatics experts are helping figure out how widespread the variant might already be in the U.S. and how quickly it could become dominant here, as it did in the U.K.

On Tuesday, Bedford answered questions about the new variant, including its potential impacts on vaccine effectiveness and development of herd immunity and whether additional measures might be needed to keep it in check.

The conversation has been edited for clarity and brevity.

Q: Detecting and monitoring the new variant requires sequencing the genomes of viruses from large numbers of infected people. How is that being done in the U.S.?

A: The U.K. early on decided to have a consolidated national approach to doing this genomic surveillance. They were able to have a few big labs do a lot of testing and then share positive specimens with a handful of big sequencing labs. In the U.S., most of public health is really at the state level. So what’s happened is that there are a handful of public health labs that are doing a good job of sequencing viruses that are collected in their state and sharing that. But there isn’t really a national strategy.

The CDC has given grants to help support academic labs and states to do this work, but it’s a bit slower than it should be. Because this work is done at the state labs, issues of personnel and resources mean that the sequencing often doesn’t end up as the top priority.

Q: The U.S. ranks 43rd in the world in the percentage of positive cases that are sequenced, and you were recently quoted in a New York Times editorial that called for a major expansion. Is anything being done?

A: The U.S. has sequenced and shared over 50,000 virus genomes, more than any country in the world, except for the U.K. However, the turnaround times have not been great. There are thousands of viruses that were shared in the database in December, but a great many of those were from specimens collected back in March.

The CDC has plans to (start) receiving specimens from the state labs and then doing the sequencing more centrally and share the data. So there are plans to have thousands more genomes sequenced every month, but I don’t know when that will come online.

Q: The first U.S. infection with the U.K. variant was reported Tuesday in a Colorado man in his 20s with no recent travel history. How prevalent do you think that variant and a similar one detected in South Africa are in the U. S.?

A: My working hypothesis is that they are here but circulating at very low levels. And if they are more transmissible, which I think is likely, then they will be expanding, and we’ll catch them when they hit some frequency threshold.

Q: Travelers from the U.K. now need a negative coronavirus test to enter the U.S. How effective do you think that will be in slowing the spread of the variant?

TB: I think it’s smart at this point. I don’t have hope that we will be able to contain the U.K. variant in the U.K. in the same way I didn’t have hope in February that we were going to contain COVID in China. But testing to reduce the number of infected individuals traveling can still slow things down.

I think it might stop mattering so much once these variants become more common here.

Q: You’ve said the new variant might be slightly less susceptible to vaccine-induced immunity, but that it isn’t different enough to completely foil existing vaccines. Why?

A: The main reason I think that is because there’s a particular mutation in the U.K. variant that removes two different (portions) of the spike protein, and that tucks in a bit of protein that was sticking out and was an antibody target. So it removes that target for antibodies.

And there was a study from a lab in Cambridge … where they took serum from people who had recovered from COVID and measured it against wild type virus and against viruses that have this deletion. And they saw that the antibodies of the recovered individuals neutralize the mutated virus significantly less than the wild type virus.

If I had to hazard a guess, I believe we could see a modest reduction, like from 95% vaccine effectiveness to 85% or so, but I don’t think it would really severely inhibit the vaccine.

Q: If this variant becomes common and lowers the overall effectiveness of the vaccines even slightly, what are the implications for the development of herd immunity?

A: I think we’ll still get there. It’s just going to be a bit more challenging.

Two weeks ago, my expectation for the U.S. and for Washington state was that by March things start to get under control, (due to) seasonality and a hundred million doses of vaccines by the end of February, theoretically. Also, people are continuing to get infected and have immunity after they recover. So you could imagine those three things combining to have an effect.

But now, that’s roughly the time frame I’d expect for the variant to start to become predominant in the U.S., given that it appeared to have emerged in London around September and became predominant around December. So it took about three months there.

Q: Will we have to change our behavior and do things differently to prevent the spread of the new variant?

A: If you look at the U.K. data, when you compare the wild type virus to the variant virus, people infected with the variant have 10 to a hundred times higher viral loads on average.

So people who are infected by the variant will be breathing out more virus than someone infected by the wild type. Public Health England had a really good … case-controlled study where they showed that for individuals infected with the wild type, 10% of their contacts ended up with COVID, whereas individuals with the variant had about 15% of their contacts ending up with COVID.

So that means that in March, or whenever the variant starts becoming predominant here, a larger proportion of household contacts and close contacts of infected people will also become infected.

But the things that are safe now should still be safe then. The same strategies that we’re using to try to limit the spread now – social distancing and wearing masks and so forth – are the right strategies. It’s just that there will be more contagiousness to deal with.

Q: What does the rapid emergence of this new variant suggest about the future? Are we going to eventually see strains that are resistant to all of vaccines?

A: It was surprising to me, and I think, to most evolutionary virologists. The evolutionary mechanism definitely appears to be selection for more transmissibility. The virus evolves to more transmissible because that’s what evolution is selecting for.

Most people haven’t yet been infected and don’t have immunity, but as we have more and more individuals with immunity from natural infection or vaccination, you do have more evolutionary pressure on the virus to evolve in ways that escape from that immunity.

However, my main expectation here comes from what we know about seasonal coronavirus, which account for 30% of common colds. We can look at their evolution and they seem to infect people every three years or so and evolve at a slightly slower rate than influenza. That suggests to me a kind of flu-like pattern where you might need to update the vaccine every two or three years, and where evolving strains might be able to reinfect people on that sort of time scale as well.