Advertisement
Nathaniel Lash and
Around the world, hope for a return to normalcy is pinned on a vaccine, the “ultimate weapon,” as it’s been called by officials like Dr. Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases. But it’s still unclear how successful a vaccine against SARS-CoV-2, the virus that causes Covid-19, can be.
A lot will depend on how the virus mutates. Broadly, there are two ways mutations can play out.
A successful vaccine could stop the virus dead in its tracks, but only if the virus doesn’t mutate its way around the shot. Here’s what scientists are watching for:
Like all viruses, SARS-CoV-2 is mutating as it passes from person to person. A “mutation” is just a change in a virus’s genetic code. Most mutations don’t really change how the virus functions.
Below is a glimpse at an imaginary virus. It’s doing what all viruses do: entering a cell, hijacking the cell’s machinery and using it to make many copies of itself.
Sometimes, small errors — or mutations — can show up in that replication. Those errors accumulate over time as the virus spreads from cell to cell and person to person.
Vaccines work by prompting the body to develop antibodies, which neutralize the virus by binding to it in a very specific way. Scientists are watching to see if mutations will affect this interaction. If they don’t, then there is hope that a vaccine won’t need constant updating.
That same process has played out with our most effective vaccines, including the one against measles.
“Measles mutates just as fast as flu and coronavirus, but the measles vaccine from 1950 still works today,” said Trevor Bedford, a biologist at the Fred Hutchinson Cancer Research Center in Seattle.
To enter a cell, the measles virus uses certain of its proteins that are unable to mutate even slightly without breaking. The vaccine targets those parts, so any mutation that would evade the vaccine would mean that the virus can’t infect other cells.
The vaccine has the measles virus cornered.
But what if the virus doesn’t get cornered like measles? If the virus mutates in a way that prevents antibodies from binding, it could make a lasting, universal vaccine difficult to create.
Antibodies, which the body produces in response to a vaccine or an infection, work by binding to specific spots on a virus called antigens. If random viral mutations alter the shape of an antigen, it can make a vaccine less effective against the virus.
“What will happen in many viruses is you’ll get infected by Strain A; your immune system learns to recognize that surface protein, but then the virus is able to mutate in such a fashion that it still performs its function but make it so that your antibodies against Strain A no longer recognize Strain B,” Dr. Bedford said.
Here’s that scenario playing out on our fictional virus: The antibodies produced by the vaccine work on one strain but can’t bind to the other, rendering the vaccine ineffective.
That’s what happens with the flu: The virus’s antigens mutate so much that they evolve into different strains, each requiring a slightly different vaccine. Scientists continuously develop vaccines to target those new strains. In spite of that, the vaccines offer only partial immunity to the various flu strains that spread each year.
If that happens with the coronavirus, researchers will have to rush to produce and administer new vaccines as novel strains of the virus naturally arise.
It also reveals another quirk with how viruses behave: Some can respond to the immunity in the population they’re trying to infect. Over time, for example, many people develop immunity to at least some strains of the flu — either through fighting off infections or by getting vaccinated. But the virus keeps spreading. Here’s how.
For a brand-new virus like SARS-CoV-2, there is no widespread immunity. This virus is encountering few immune hosts who could halt its spread. Since the virus doesn’t need to change to survive, mutations that could modify the shape of the antigens — if they exist at all — are likely rare, and will stay rare.
But if people become immune to the dominant strain, either by fighting off the virus or through vaccination, the game changes. Versions of the virus with mutations that get around the population’s immunity are more likely to spread, and can then develop into new strains.
Scientists know that SARS-CoV-2 is mutating.
Among the thousands of samples of the long strand of RNA that makes up the coronavirus, 11 mutations have become fairly common. But as far as we know, it’s the same virus infecting people all over the world, meaning that only one “strain” of the virus exists, said Peter Thielen, a molecular biologist with the Johns Hopkins Applied Physics Laboratory.
Only one of those common mutations affects the “spike protein,” which enables the virus to infect cells in the throat and lungs. Efforts to produce antibodies that block the spike protein are central to many efforts to develop a vaccine. Since the spike protein has changed little so far, some scientists believe that’s a sign that it can’t alter itself very much and remain infectious.
There’s still a lot about the virus we don’t know. We don’t even know if people are immune to the virus if they’ve caught it already, nor how long that immunity could last, though work is well underway to understand these things.
Mr. Thielen says it is still unclear how those mutations in the genome will ultimately affect countermeasures like a vaccine.
“We just have to keep looking,” he said.
Nathaniel Lash is a graphics reporter in Opinion @Nat_Lash.
Tala Schlossberg is a visual journalism fellow in Opinion @TalaSchlossberg.
Follow The New York Times Opinion section on Facebook, Twitter (@NYTopinion) and Instagram.
Advertisement