Coronavirus variants have been popping up around the globe—which is no surprise, once you understand how mutant germs work. But with ambitious vaccination programs underway, the big question is whether these variants will make vaccines less effective.

It’s normal for viruses to mutate when they make copies of themselves, says Brianne Barker, professor of biology at Drew University in Madison, New Jersey. In fact, from March to September, scientists found an average of two new coronavirus variations emerged every month.

“Variations of the virus are made every day. Then, there’s a competition for which can reproduce the best and fastest,” Barker explained. Some genetic alterations will make the coronavirus weaker, or in evolutionary terms, less “fit.” But eventually, some of these changes will make it better at infecting its new human hosts.

This unfortunate scenario is now a reality. On Friday, U.K. officials announced the variant spreading there—believed to be around 50% more transmissible—could also be up to 30% more deadly than the original strain, according to a preliminary assessment.

“If you took somebody in their 60s, the average risk is that for 1,000 people who got infected, roughly 10 would be expected to unfortunately die with the [old] virus,” Patrick Vallance, the U.K.’s chief scientific advisor. “With the new variant, roughly 13 or 14 people might be expected to die….You will see that across the different age groups as well.”

And two studies released on Tuesday show that other coronavirus variants pose a more significant risk to our immune defenses than previously hoped. The variants can partially bypass our natural immunity, as well as the protection generated by the frontrunner vaccines made by Pfizer-BioNTech and Moderna.

“The sort of headline ‘95% effectiveness’’ that we've been hearing about might begin to diminish,” said Paul Bieniasz, a virologist and a professor at The Rockefeller University in New York City. He co-authored one of the new reports, which were posted as preprints ahead of peer-review in academic journals.

Luckily, in the short term, these current vaccines will still neutralize the coronavirus variants we’ve identified so far. But this research provides the first concrete indications that our immunity against COVID-19 could lose effectiveness over time—and that the vaccine formulas may need to be updated periodically to cope.

Here’s what you need to know to prepare for the future.

Why do scientists keep using the word “variant?”

When researchers spot a new mutation in a virus, it is often unclear whether the change makes a substantial difference in how it causes disease. Scientists use the term variant or “variant of concern” to distinguish one such mutant from another—especially when one starts showing signs of being more potent.

That’s what happened over the last five or so months. Scientists spotted three aberrant but similar pedigrees in separate spots around the world: The U.K., South Africa, and Brazil. Each harbors about 20 noteworthy mutations, some of which overlap.

“When you start to see the same mutation, over and over, it becomes suggestive that it could be an adaptation of some kind of benefit to the virus,” says Stephanie Spielman, assistant professor of biological sciences at Rowan University in Glassboro, New Jersey.

So far, at least three such adaptations have emerged in multiple countries. One is called N501Y, and it involves the coronavirus’s spikes—the proteins that coat the germ and allow it to break into our cells. This alteration is found in the variants hailing from both the U.K. and South Africa, which have eight and nine differences located on their spikes, respectively. Two others are named E484K and K417N. They feature in the variants from South Africa and Brazil.

Scientists are working tirelessly to answer two big questions about this mutant collection:

Will these variants impact the vaccine? Will they make the disease more infectious or severe?

Paul Bieniasz, a virologist and a professor at the Rockefeller University in New York City, has found that this trio of mutations—N501Y, E484K, and K417N—can sneak by some of the antibodies that destroy the virus.

What his lab and others have learned over months is that certain types of antibodies are commonly generated during a natural infection and after vaccination. It turns out that those antibodies neutralize the virus by precisely targeting the exact region in the spike where those three mutations occur.

“This is a hotspot. It's a very important spot for the virus to attach to [cell] receptors,” Bieniasz said. Other recent research supports these findings, showing that in those who have already had COVID-19, the E484K mutation may keep antibodies from recognizing the virus, making reinfection more likely.

This trio of mutations, however, isn’t acting alone. The same day the Rockefeller study dropped, South African researchers released a similar report that collected convalescent plasma— antibody-packed goop found in blood—from 44 people infected during the country’s first wave. Plasma from 90% of these cases showed reduced immunity to South Africa’s variant. Half of the cases showed total immune escape, meaning the antibodies had been rendered useless. Vaccinations offer better protection than natural infection because they provide a more comprehensive set of antibodies, but it’s still not good news.

While the U.K. variant poses less of a threat toward escaping our immunity, it originally appeared to be far more contagious than the original strain of coronavirus. Just by being more infectious or circumventing our immune systems, more people were at risk of becoming severely ill. Friday’s preliminary announcement from Downing Street raises the stakes if this variant increases mortality, too.

The Centers for Disease Control and Prevention has published a study suggesting that the U.K. variant could become dominant in the United States by March—imperiling healthcare systems that are already overwhelmed.

So, the vaccines are kaput? Should I still take one?

So far, the vaccines remain highly effective, but we’re now in a race against time before the shots lose their potency.

The situation echoes what happens every year with the flu. Drugmakers concoct a new version of the vaccine to adjust for mutations in the influenza virus, which accumulate steadily over the seasons. Many other diseases require frequent vaccinations because of this kind of viral evolution.

Further evidence of this potential fate comes from two other recent studies that found the spikes on cold-causing coronaviruses—cousins of SARS-CoV-2, the virus that causes COVID-19—also regularly evolve. Both papers suggest that coronavirus immunity dissipates over a few years.

Thankfully, Pfizer and Moderna’s vaccines work by delivering messenger RNA, material that can easily be tweaked to target subtle changes in the coronavirus. Updating the vaccine will require time to manufacture and distribute new versions—but Moderna designed their current successful vaccine in just two days.

“If a vaccine-resistant variant of SARS-CoV-2 were to emerge, current vaccines could be tweaked to address any new mutations,” Phil Dormitzer, one of Pfizer’s top viral vaccine scientists, said in a statement to Gothamist. “We are laying the groundwork to respond quickly if a future variant of SARS-CoV-2 is unresponsive to existing vaccines. Any changes to the vaccines would have to follow solid clinical observations that a new variant is spreading among people already immunized against COVID-19.”

An early study from Pfizer and BioNTech suggests their vaccine could defend against the U.K. variant, and they are also conducting studies to monitor the vaccine’s real-world effectiveness against circulating SARS-CoV-2 strains. Moderna did not reply to a request for comment.

These vaccines also appear far more adept at preventing disease than influenza vaccines, which are typically only 40-60% effective. The Rockefeller study found the variants reduced the effectiveness of our best antibodies by 5- to 10-fold. Even if the first rounds of COVID-19 vaccines gradually lose their potency, they can still help save lives.

“There’s a thing called a cushion effect,” Dr. Anthony Fauci, the director of the National Institute of Allergy and Infectious Diseases, said at a White House press briefing on Thursday. “You’re still well above the line of not being effective, so there’s that cushion. Even though it’s diminished somewhat, it still is effective.”

But Bieniasz strongly suspects that the variants will eventually substantially diminish the vaccines’ abilities to stop the virus’s spread. That would emphasize the need to social distance and wear masks until the vaccines can be updated.

“The first signs of a vaccine just beginning to be a bit less efficacious might not come in terms of vaccine recipients getting sick, but might come in terms of them being able to transmit the virus onto others,” he said. Complicating matters is that we don’t have good data yet on how much the prevailing vaccines reduce transmission. But a recent news report from Israel, where a third of the population has been immunized, stated one dose of the Pfizer vaccine could curb transmission by 50%.

The real concern, Spielman says, is what might happen going forward. “The truth is ten mutations could be fine—or we could be one mutation away from the vaccine not working.”

So, what should you do now? How do we stop these variants?

Besides getting vaccinated, social distancing, and mask wearing, the nation could protect itself with greater investments in coronavirus testing—namely genome sequencing. Ideally, the U.S. would be analyzing as many samples as possible from COVID-19 cases to track mutations.

The U.S. has significantly lagged behind other countries in genomic surveillance, in spite of having the most coronavirus cases—more than 24 million—in the world. When the U.K. variant was first identified, British researchers had sequenced 137,000 genomes, nearly 50% of the world’s total. By comparison, despite its massive caseload, the U.S. had sequenced less than 20%. That’s dangerous when each new case represents an opportunity for the virus to multiply and mutate.

Without robust genomic surveillance, we’re blind to where the variants are thriving. An analysis released this week predicts the U.K. variant has likely been circulating in the US since mid-November. It’s a problem that may get worse: Just this week, researchers at Cedars-Sinai reported a new variant in California—one they are calling CAL.20C.

Carl Bergstrom, professor of biology at the University of Washington, recently raised the alarm about this exponential threat.

“Just as this autumn we didn't know about the more transmissible strains that were beginning to spread in our midst,” he tweeted, “there is every reason to expect there are now a number of more recent mutations of concern that arose this winter, but we have yet to detect.”

Lois Parshley is a freelance journalist covering COVID-19. Follow her on Twitter @loisparshley.