Vaccines Are Effective Against the New York Variant, Studies Find

For weeks, New Yorkers have witnessed the alarming rise of a homegrown variant of the coronavirus that has kept the number of cases in the city stubbornly high. City officials have repeatedly warned that the variant may be more contagious and may dodge the immune response.

On that second point, at least, they can now breathe easier: Both the Pfizer-BioNTech and Moderna vaccines will effectively prevent serious illness and death from the variant, two independent studies suggest.

Antibodies stimulated by those vaccines are only slightly less potent at controlling the variant than the original form of the virus, both studies found.

“We’re not seeing big differences,” said Michel Nussenzweig, an immunologist at Rockefeller University in New York and a member of the team that published one of the studies on Thursday.

The bottom line? “Get vaccinated,” he said.

The results are based on laboratory experiments with blood samples from small numbers of vaccinated people and have not yet been peer-reviewed. Still, they are consistent with what is known about similar variants, several experts said, and they add to a growing body of research that suggests that the two main vaccines in the United States are protective against all of the variants identified so far.

“The take-home message is that the vaccines are going to work against the New York variant and the South African variant and the U.K. variant,” said Nathan Landau, a virologist at N.Y.U.’s Grossman School of Medicine who led the study.

The vaccines spur the body to mount an expansive immune response, with thousands of types of antibodies and several types of immune cells. One subset of these immune fighters, called neutralizing antibodies, is essential for preventing infection. But even when neutralizing antibodies are in short supply or even absent, the rest of the immune system may marshal enough of a defense to fend off serious illness and death.

In both new studies, neutralizing antibodies from vaccinated people were better at thwarting the virus than those from people who developed antibodies from being sick with Covid-19. Direct comparison of the two sets of antibodies offered a possible explanation: Antibodies from vaccinated people are distributed across a broader range of parts of the virus, so no single mutation has a big impact on their effectiveness — making vaccines a better bet against variants than immunity from natural infection.

The variant first identified in New York, known to scientists as B.1.526, raced through the city after its initial discovery in November. It accounted for one in four diagnosed cases by November and nearly half of cases as of April 13. The variant that brought Britain to a standstill, B.1.1.7, is also circulating widely in New York. Together, the two add up to more than 70 percent of coronavirus cases in the city.

The worry about the variant identified in New York has centered on one form of it, which contains a mutation that scientists are calling Eek. The Eek mutation subtly alters the shape of the virus, making it difficult for antibodies to target the virus and, as a result, undercutting the vaccines.

In the second study, Dr. Landau’s team found that the Pfizer and Moderna vaccines are only marginally less protective against the variant that devastated Britain and against forms of the variant discovered in New York that don’t contain the Eek mutation.

Several laboratory studies have shown that antibodies induced by the Pfizer and Moderna vaccines are slightly less powerful against a third variant, one identified in South Africa, which also contains Eek. Other vaccines fared worse. South Africa suspended use of the AstraZeneca vaccine after clinical trials showed that the vaccine did not prevent mild or moderate illness from the variant that was circulating there.

“It already started out as a lower level in terms of the immunity that it generated,” Dr. Nussenzweig said of the AstraZeneca vaccine. Referring to the Pfizer and Moderna shots, he said, “We’re so lucky in this country to have these vaccines compared to the rest of the world.”

Florian Krammer, an immunologist at the Icahn School of Medicine at Mount Sinai who was not involved in either of the new studies, said he was more concerned about other countries’ vaccine programs than about the variants themselves.

“I am less concerned about variants than I was two months ago,” he said, but added: “I’m worried about countries that don’t have enough vaccine and that don’t have that vaccine rollout. I’m not worried anymore about the U.S., honestly.”

Dr. Landau’s team also tested monoclonal antibodies used to treat Covid-19 against the variants. They found that the cocktail of monoclonal antibodies made by Regeneron worked as well against the variant discovered in New York as against the original virus.

The studies are reassuring, but they indicate that the Eek mutation is one to watch, said Jesse Bloom, an evolutionary biologist at the Fred Hutchinson Cancer Research Center in Seattle.

“This could certainly be a step toward the virus becoming somewhat more resistant to infection- and vaccine-mediated immunity,” Dr. Bloom said. “I don’t think it’s something that people need to immediately become alarmed about, but it definitely impresses us as important.”

Dr. Bloom led the analysis comparing vaccine-induced antibodies with those produced by natural infection. He found that the most powerful antibodies bind to multiple sites in a key part of the virus. Even if a mutation affects the binding in one site in this region, antibodies that target the remaining sites would still be protective.

Antibodies induced by the vaccine cover many more sites across this region than those from natural infection — and so are less likely to be affected by a mutation in any one site.

The study looked only at antibodies stimulated by the Moderna vaccine, but the results are likely to be the same for the Pfizer-BioNTech vaccine, he added.

“This could potentially be a good thing as the virus is creating mutations,” Dr. Bloom said.

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