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Five reasons why you don’t need to panic about coronavirus variants

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2. The immune response is robust 

Scientists testing vaccine efficacy often focus on antibodies and their ability to block the virus from infecting cells. In lab experiments, they mix blood from people who have been infected or vaccinated with cells in a dish to see if antibodies in the blood can “neutralize” the virus. These experiments are easy to perform. But antibodies are “a very narrow slice of what the immune response might be” in the body, says Jennifer Dowd, an epidemiologist and demographer at the University of Oxford. 

Immune cells called T cells also help keep infections in check. These cells can’t neutralize the virus, but they can seek out infected cells and destroy them. That helps protect against severe disease. And data from people who’ve had covid-19 suggests that T-cell response should provide ample protection against most of the SARS-CoV-2 variants. 

3. When vaccinated people do get infected, the shots protect against the worst outcomes

A vaccine that can block infection is wonderful. But “the most important thing is to keep people out of the hospital and out of the ground,” says Friedrich. And there’s good evidence that the current vaccines do exactly that. In South Africa, one dose of the Johnson & Johnson vaccine provided 85% protection against covid-19-related hospitalizations and deaths. At the time, 95% of cases were caused by the B.1.351 variant. In Israel, where B.1.1.7 has become the dominant strain, two doses of Pfizer offered 97% protection against symptomatic covid-19 and hospitalizations linked to covid-19. 

4. The same mutations keep popping up 

Once the virus enters a cell, it begins to replicate. The more copies it makes, the greater the likelihood that random errors, or mutations, will crop up. Most of these copying errors are inconsequential. A handful, however, might give the virus a leg up. For example, a spike-protein mutation known as D614G appears to help transmission of SARS-CoV-2. Another, E484K, might help the virus evade the body’s antibody response. If the viruses carrying these advantageous mutations get transmitted from one person to the next, they can start to outcompete the viruses that lack them, a process known as natural selection. That’s how the B.1.1.7 variant, which is more transmissible, became the predominant strain in the US. 

In the case of SARS-CoV-2, the mutations that improve the virus keep popping up in different parts of the globe, a phenomenon known as convergent evolution. “We are seeing the same combinations evolving over and over and over again,” says Vaughn Cooper, an evolutionary biologist at the University of Pittsburgh. Imagine a game of Tetris, Cooper writes in a recent story for Scientific American. “A limited number of building blocks can be assembled in different ways, in different combinations, to achieve the same winning structures.”

Cooper and some other researchers see this evidence of convergent evolution as a hopeful sign: the virus may be running out of new ways to adapt to the current environment. “It’s actually a small deck of cards right now,” he says. “If we can control infections, that deck of cards is going to remain small.” 

5. If the effectiveness of the vaccines begins to wane, we can make booster shots. 

Eventually, the current vaccines will become less effective. “That’s to be expected,” Chandran says. But he expects that to happen gradually: “There will be time for next-generation vaccines.” Moderna has already begun testing the efficacy of a booster shot aimed at protecting against B.1.351 (first identified in South Africa). Last week the company released the initial results. A third dose of the current covid-19 shot or a B.1.351-specific booster increased protection against the variants first identified in South Africa and Brazil. But the new variant-specific booster prompted a bigger immune response against B.1.351 than the third dose of the original shot. 

That’s a relief for a couple of reasons. First, it demonstrates that variant-specific boosters can work. “I think the feasibility of these RNA-based vaccines to produce boosters is the achievement of our lifetime,” Cooper says. 

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