No, the coronavirus isn't becoming more contagious or less deadly — it's already 'very successful at what it's doing,' a geneticist says

People wear face masks as they attend the live broadcast of Pope Francis' Sunday Angelus prayer at Saint Peter's Square in Vatican City, March 8, 2020.Antonio Masiello/Getty Images

• Viruses like the coronavirus can change over time as they accumulate genetic errors, or mutations.
• A group of Italian doctors suggested the coronavirus has changed to become less lethal.
• Some research also shows that a mutated strain of the virus is more transmissible than the original in cells.
• But a geneticist that tracks the virus's spread told Business Insider that it has yet to mutate in a meaningful way, and there's no evidence it has gotten weaker or more contagious.
• Visit Business Insider's homepage for more stories.

Experts continue to throw out conflicting ideas about whether the coronavirus has changed. Some Italian doctors say it's gotten weaker over time. A group of researchers has suggested the opposite: that a mutated version of the virus became dominant worldwide because it's more transmissible than the original. 

All viruses, including the coronavirus, change over time by accumulating mutations as they replicate. But according to Emma Hodcroft, a geneticist at the Nextstrain project, there's still no evidence this virus changed in any significant way — not to become less deadly, and not to be more contagious.

The Nextstrain project has been tracking changes in the coronavirus for months. So far, Hodcroft's team has collected and sequenced the genome of thousands of virus samples collected around the world since December 2019.

Geneticists differentiate these samples into five clades — the term for groups of virus samples that have descended from a common ancestor — characterized by mutations that have accumulated over time in one or more of a dozen genes.

But none of those mutations have meaningfully changed how lethal or infectious the coronavirus is, Hodcroft said. 

Humans have not exerted pressure on the virus to change

It's easy to think that humanity's attempts to control the coronavirus's spread via social distancing, mask wearing, and lockdowns may have applied evolutionary pressure on the virus. Given impediments to its spread, this line of logic suggests, perhaps the virus might evolve to improve how it passes between people. 

But according to Hodcroft, the virus has no significant impetus to change right now.

"The virus is very successful at what it's doing — most people who get infected don't die. They pass along the virus to a new host and recover," Hodcroft said. "It's current strategy has helped it cover the whole world in months."

If the original strain of the coronavirus killed its host within a few days, then perhaps it might have mutated over time to not kill as quickly, she added — that would give it more opportunities to jump to new hosts. But on average, people die of COVID-19 18 to 19 days after symptoms start, according to a study from Wuhan, China.

Alternatively, if social distancing were having an effect, Hodcroft said, the coronavirus might mutate to become more infectious "to overcome barriers we put in its way."

Research has in fact shown that a mutated coronavirus strain became dominant worldwide — one that appears to be more transmissible between human cells than the original virus. But Hodcroft said the strain might simply have gotten lucky, since it ended up being the version that spread to countries in Europe and North America. Many of those countries did not enact lockdowns for weeks after their first cases appeared, which allowed that version of the virus to proliferate.

Plus, scientists still aren't sure whether observations at the cellular level apply to real people.

"We don't know how things we see in a lab scale up to a size of a full human. Transmissibility in cells and people are completely different ballgames," Hodcroft said.

She added that such mutations, though possible, "happen over decades or centuries."

'This is still a killer virus'

In a June op-ed, 10 Italian doctors suggested that the coronavirus was weakening and had changed to be less lethal.

The "virus from the clinical point of view no longer exists" in Italy, they wrote, citing a marked reduction in coronavirus cases and hospitalizations. The op-ed also noted that viral loads — how much of the virus is present in swabs — from many Italian patients were so negligible that patients were not even contagious. 

"The concentration of viral RNA on the swab is so small that it does not infect anything," Giuseppe Remuzzi, one of the op-ed co-authors, told Politico last week. 

But Hodcroft said "there isn't any validity to those claims."

In fact, she added, it's "misleading for Italian doctors to say this when they're looking at only Italian patients."

Michael Ryan, the executive director of WHO's Health Emergencies Program, similarly warned in June: "We need to be exceptionally careful not to create a sense that all of sudden the virus, by its own volition, has now decided to be less pathogenic. This is still a killer virus."

The more likely explanation for the trend the Italian doctors have observed, Hodcroft said, is that in March, Italy's healthcare system was strained, so most patients admitted to the hospital had very severe cases. At that time, about 6,500 new cases were being reported per day in Italy. But by the end of May, the number had dropped to about 300. That may have enabled more Italians with milder cases to get care, which could explain the lower viral loads in swab tests.

Indeed, two studies found that people who develop more severe respiratory issues linked to COVID-19 have higher viral loads when admitted to the hospital relative to people with mild cases.

"As the pandemic slows down, more of the general population is getting tested, so you'll probably pick up more people with mild symptoms," Hodcroft said. "If you don't account for that, that could lead you to believe the virus has become less severe."

Adam Payne contributed reporting to this story.

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