India’s Covid-19 crisis: The “double mutation” issue isn’t what you think

“I don’t know why the press came up with that term.”

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The Covid-19 situation in India is dire. Hospitals are reportedly closing their gates, unable to accept any more patients. Journalists on the ground say the hospitals that do have room are only taking patients who come with their own oxygen because the hospitals have run out.

And about halfway through a story about the crisis the New York Times published on Tuesday was this terrifying statement:

“A new variant known here as “the double mutant” may be doing a lot of the damage. The science is still early but from what we know, this variant contains one mutation that may make the virus more contagious and another that may make it partially resistant to vaccines.”

Fortunately, while research on this so-called “double-mutation” is still in its early stages, experts say it’s not as alarming or novel as the name and framing suggests. In fact, they don’t even think it should be called a “double-mutation” variant at all. The actual name of the variant is B1617 — and the experts say we’d all do well to call it that instead.

B1617 likely contributes to the transmissibility of Covid-19 but not the severity of the disease. It’s one piece of a horrible puzzle, but a less important piece compared to crisis drivers like relaxed restrictions and low vaccine coverage.

What is a “double mutation”?

“I don’t know why the press came up with that term,” Amesh Adalja, a senior scholar at the Johns Hopkins Center for Health Security, tells Inverse. “All the variants have double mutations, in fact, they all have more mutations than that. The South Africa variant probably has seven or eight.”

When considering the danger of variants, it’s useful to consider two questions:

  • Are the mutations new — have we seen them in other variants and understand what they can and can’t do?
  • Do they affect a meaningful aspect of the virus, like transmissibility, illness severity, and vaccine evasion? Not all mutations will.

So back to B1617. What do we know about the mutations?

Like most variants, B1617 has more than two mutations. But it gets its (however misguided) name because of two specific mutations within that bunch:

  • One of the mutations is called L452R, which is also found in the California variant, B.1.427/B.1.429.
  • The second mutation is called E484Q. It’s very similar to the mutation found on the spike protein in the Brazil and South Africa variants (called E484K)

Does the “double mutation” increase transmission?

It’s very likely that it does. A study published on April 20 in Cell found that the same mutation in the California variant increased transmission up to 20 percent.

Given that B.1617 has an identical mutation, it’s safe to assume it has the same increase in transmissibility.

Does the “double mutation” increase severity?

It’s too soon to say definitively, but early indications suggest the second mutation, E484Q, will function similarly to the E484K mutation found in Brazil and South Africa — meaning it doesn’t appear to increase illness severity.

However, the concern with the E484K mutation is its increased ability to slip past the body’s immune defenses (more on that below).

That said, anytime you have a variant that’s more transmissible, more people will be infected and more people are likely to get ill. That’s a good reason to still protect yourself and others as much as possible by social distancing, masking, and getting vaccinated as soon as you can.

What do we know about variants and vaccines?

Here’s the good news: vaccines provide much stronger antibody protection than what’s caused by naturally contracting the virus. Every indication suggests that the vaccines should still provide really solid protection against severe illness or death.

The main question with variants, says William Schaffner, an expert in infectious diseases at Vanderbilt University Medical Center, is: Do the vaccines work? “That’s the most important question for ourselves, and for people around the world. So far, the vaccines that we have worked,” he says.

Adalja stresses a vaccine-related point that is often missed in these discussions: “When you see a story that says ‘oh with the antibody titers, there was a twofold reduction in neutralization,’ what you need to ask yourself is: is that clinically relevant?”

The immunity vaccines provide have an enormous cushion. Just because there might be a reduction in antibody potency, that doesn’t necessarily mean you’re less protected.

It’s a bit like taking Tylenol for a mild headache as opposed to extra strength Tylenol. For most mild headaches, it doesn’t really matter if you take the extra strength or not, it’s going to work either way.

Another thing the media often misses, Adalja says, is the role of T-cells. Most of those tests are only looking at one arm of the immune system, he says. “They’re not looking at T-cells. And T-cells play a major role in immunity induced by a vaccine.”

But this comfort is reserved for people with access to vaccination. And that’s a huge issue right now in India.

If the B.1617 variant isn’t responsible for the crisis in India, what is?

Opening too soon and a lack of vaccinations, Schaffner says.

“The government decided to open up and to put aside caution, such as social distancing and avoiding large groups,” he says. Combine that with a very low vaccination rate — currently, about 1.7 percent of the population is fully vaccinated — and you’ve got a real crisis.

As of April 27th, only 1.7 percent of India’s population had been fully vaccinated.

Our World Data

The new variant is likely contributing to that crisis, Schaffner says, but it’s far from the primary reason.

Is the “double mutation” found in other countries?

Yes, according to the World Health Organization, variant B1617 has been found in at least 17 countries.

Variants are a natural part of a virus’s evolution. And with this pandemic, we’ve given the virus hundreds of millions of chances to evolve. Fortunately, the best way to quash these variants is by getting vaccinated.

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