The delta variant of the coronavirus can evade antibodies that target certain parts of the virus, according to a new study published Thursday in Nature. The findings provide an explanation for diminished effectiveness of the vaccines against delta, compared with other variants.
The variant, first identified in India, is believed to be about 60% more contagious than alpha, the version of the virus that thrashed Britain and much of Europe earlier this year, and perhaps twice as contagious as the original coronavirus. The delta variant is now driving outbreaks among unvaccinated populations in countries like Malaysia, Portugal, Indonesia and Australia.
Delta is now the dominant variant in the United States. Infections in the country had plateaued at their lowest levels since early in the pandemic, though the numbers may be rising. Still, hospitalizations and deaths related to the virus have continued a steep plunge. That is partly because of relatively high vaccination rates: 48% of Americans are fully vaccinated and 55% have received at least one dose.
But the new study found that delta was barely sensitive to one dose of vaccine, confirming previous research that suggested that the variant can partly evade the immune system — although to a lesser degree than beta, the variant first identified in South Africa.
French researchers tested how well antibodies produced by natural infection and by coronavirus vaccines neutralize the alpha, beta and delta variants, as well as a reference variant similar to the original version of the virus.
The researchers looked at blood samples from 103 people who had been infected with the coronavirus. Delta was much less sensitive than alpha to samples from unvaccinated people in this group, the study found.
One dose of vaccine significantly boosted the sensitivity, suggesting that people who have recovered from COVID-19 still need to be vaccinated to fend off some variants.
The team also analyzed samples from 59 people after they had received the first and second doses of the AstraZeneca or Pfizer-BioNTech vaccines.
Blood samples from just 10% of people immunized with one dose of the AstraZeneca or the Pfizer-BioNTech vaccines were able to neutralize the delta and beta variants in laboratory experiments. But a second dose boosted that number to 95%. There was no major difference in the levels of antibodies elicited by the two vaccines.
“A single dose of Pfizer or AstraZeneca was either poorly or not at all efficient against beta and delta variants,” the researchers concluded. Data from Israel and Britain broadly support this finding, although those studies suggest that one dose of vaccine is still enough to prevent hospitalization or death from the virus.
The delta variant also did not respond to bamlanivimab, the monoclonal antibody made by Eli Lilly, according to the new study. Fortunately, three other monoclonal antibodies tested in the study retained their effectiveness against the variant.
In April, citing the rise of variants resistant to bamlanivimab, the U.S. Food and Drug Administration revoked the emergency use authorization for its use as a single treatment in treating COVID-19 patients.
Separately, Pfizer announced Thursday that it was developing a version of its vaccine that targets the delta variant and expects to launch clinical trials in August.
The company also reported promising results from studies of people who received a third dose of the original vaccine. A booster given six months after the second dose increases the potency of antibodies against the original virus and the beta variant by fivefold to tenfold, the company said in a news release.
Antibody levels may decline six months after immunization, Pfizer said, and booster doses may be needed to fend off variants. But antibodies are not the only part of the body’s immune response, and other studies have suggested that immunity induced by full vaccination is likely to remain robust for years, even against variants.
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