Mutating Covid doesn’t spell doom for vaccines
From South Africa to Brazil to California, the list of locations linked to new strains of the coronavirus is growing — and so are concerns that viral variants could undo the vaccine rollout.
The worries come at a time when most Americans still haven’t received a Covid-19 vaccine. That could change by the end of May, when President Joe Biden says there will be enough vaccine for all adults in the US But by then, new and faster-spreading coronavirus strains will likely account for nearly all cases.
Does that mean this whole effort is for naught? Not according to local researchers with a deep understanding of viruses and the immune system. They say there’s ample evidence that current vaccines work well against several of the well-known variants, and that immunity is never an all-or-nothing affair.
Manufacturers and federal regulators have signalled that updating current vaccines to keep pace with new strains will be relatively straightforward. Some of that work is already happening.
‘‘On a one to 10 scale, my concern about variants is two or three,’’ said Dr Mark Sawyer, an infectious disease expert at Rady Children’s Hospital who served on the panels that recommended that the Food and Drug Administration authorise the Moderna, Pfizer and Johnson & Johnson vaccines.
‘‘I am worried about them. They could create problems – they could create big problems. But at the moment, based on what we know, they look like most of them are going to be manageable.’’ The emergence of new strains means the coronavirus is doing what all viruses do: mutating.
Each time a virus infects a cell, it copies its genetic material. But that’s not a perfect process. Given enough time, some copies will have a few random errors, or mutations – a bit like how you’re bound to make a few typos after transcribing the same document 20 times.
Most mutations don’t help a virus. Some might hurt it. But every now and then, a mutation lets a virus spread more easily from cell to cell or person to person. And viral variants with a competitive edge will eventually outnumber less successful strains.
It’s survival of the fittest, on a microscopic scale.
‘‘Viruses are clever creatures,’’ said Dr Douglas Richman, a UC San Diego virologist. ‘‘They accelerate Darwinian evolution.’’ That’s why it was a matter of time before the coronavirus mutated in ways that made it more infectious. Many of the new variants have mutations that help the virus latch more tightly onto cells before slipping inside them. Others are less vulnerable to antibodies – Y-shaped proteins that can glom onto a virus’s surface and block infection.
But these mutations rendered vaccines useless.
One of the first variants to fuel fears was detected in the UKlast fall. The variant, also known as B.1.1.7, has since been spotted in San Diego, and researchers expect it to eventually account for nearly all Covid-19 cases in the county.
Scientists reported in late January that antibodies made by people who received the Pfizer vaccine blocked the UK variant and the original strain found in Wuhan, China, from infecting labgrown cells about equally well. The same is true of Moderna’s vaccine.
By comparison, antibodies from people who’d gotten the Moderna and Pfizer vaccines were less effective against the so-called South Africa strain. That’s likely also the case for a strain first identified in Brazil, which shares several key mutations.
Real-world trial data from a different vaccine, made by pharma giant Johnson & Johnson, tell a similar story. The company’s vaccine was 72 per cent effective in the US, compared to 66 per cent and 57 per cent in Latin America and South Africa, respectively.
It’s likely no accident the vaccine was less effective in regions where some of the more concerning variants are abundant, says Erica Ollmann Saphire, a haven’t researcher at La Jolla Immunology. But the findings also underscore an important point: Immunity isn’t black or white.
‘‘The immune response is not really like a simple on-off light switch,’’ Saphire said. ‘‘It’s like a whole panel of dimmer switches. You have lots of options and lots of lights, and if one dims a little, the others might still be on.’’ That’s because vaccines spark immune responses against many different regions of a virus, not a single spot, launching a salvo of antibodies to stop infection and an army of T cells to kill infected cells before they spew out more virus.
A diversified, multipronged attack makes it less likely that any one mutation (or several) will thwart an immune response.
‘‘Most of those antibodies and most of those T cells are still going to work,’’ said Saphire, who leads an international effort to test more than 200 antibody therapies against various strains of the coronavirus.
Of all the recent reports, the most concerning to date found that AstraZeneca’s Covid-19 vaccine was 21 per cent effective in a group of 2,000 South Africans – and just 10 per cent against the fast-spreading viral strain first found in that nation.
But while the study prompted the South African government to stop its rollout of the AstraZeneca vaccine, the country simply pivoted to using doses from Johnson & Johnson.
It’s helpful to understand what vaccine ‘‘effectiveness’’ means when interpreting these numbers. When the FDA says that any coronavirus vaccine must be at least 50 per cent effective, the agency is referring to how well the vaccine compares against placebos in preventing all Covid-19 symptoms – even a mild headache or a cough.
But keeping people alive and out of the hospitals is arguably the key to restoring some semblance of prepandemic normalcy. And by that measure, Covid-19 vaccines are highly effective: Not one person vaccinated in the Johnson & Johnson, AstraZeneca, Pfizer or Moderna trials has died of Covid-19. – TNS