‘Good Read From An Immunologist’ Post Misstates Reasons for COVID-19’s Virulence

A viral Facebook post argues the mutation rate of the coronavirus is responsible for its pandemic spread. There is no scientific support for that notion.

  • Published 23 March 2020
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Copied-pasted-and-shared social media posts allegedly written by anonymous experts have been a central feature of the misinformation epidemic associated with the COVID-19 coronavirus disease pandemic. These posts, which frequently promote suspect advice or inaccurate information, evolve into multiple, slightly modified versions and have frequently gone viral on social media platforms. 

At issue here is one such post displayed below, which has been attributed to, among others, “an immunologist at Johns Hopkins University.” The post usually begins this way: “Feeling confused as to why Coronavirus is a bigger deal than Seasonal flu? Here it is in a nutshell. I hope this helps. Feel free to share this to others who don’t understand… It has to do with RNA sequencing…. I.e. genetics.”

The post makes several points, but only a few are accurate.

A majority of the claims rest on the false assumption that the coronavirus mutates at a faster rate than other viruses. Below we will go through the post point-by-point.

rna sequencing coronavirus

‘All Human Virus’

The post asserts that, unlike the seasonal flu, this novel coronavirus mutated from a viral strain originally found in an animal and therefore no human’s immune system recognizes the virus. This differs from the seasonal flu, according to the post’s author, as most humans have some innate level of immunity to influenza strains in general. This is true, according to experts.

Matt Koci, a professor of immunology, virology, and host-pathogen interactions at North Carolina State University told us by email that while “biology is more complicated than that,” the “lack of no one in the human population having any prior immunity to is a major factor to why this is so much worse than seasonal flu.” Another factor, he told us, is that a few anti-viral drugs have been developed that blunt the impact of some influenza strains, but no such tool exists for the coronavirus.

Animal-to-Human Mutation in ‘Just Two Weeks’

The post asserts that mutations in the RNA or DNA of a virus sometimes allow for animal-to-human transfer, but not human-to-human transfer. It then implies a second mutation event is required to allow for human-to-human transfer, and therefore a possible pandemic, to occur:

Now, here comes this Coronavirus. It existed in animals only, for nobody knows how long. But one day, at an animal market in Wuhan China, in December 2019, it mutated and made the jump from animal to people. At first, only animals could give it to a person. But here is the scary part. In just TWO WEEKS, it mutated again and gained the ability to jump from human to human. Scientists call this quick ability, “slippery”.

While most viruses mutate multiple times in the process that allows transfer between animal-human and then human-human, “there is no data that I’m aware of that supports the details in this statement,” Koci told us. “We still don’t know what animal it ‘jumped from’ so there is no way to know how long it took before it evolved the ability to move from person-to-person,” he explained. The virus most closely resembles a coronavirus found in bats.

In fact, this virus may have been pretty much perfectly set up to infect humans right off the bat, so to speak, and therefore would not have required the alleged multiple quick mutations to produce human-to-human transfer. Speaking to Ed Young in The Atlantic, Matthew Friedman of the University of Maryland School of Medicine explained that this novel coronavirus differs from the coronavirus that caused the 2003 SARS outbreak because this one required no modifications to thrive in human cells after its jump from animal to human. Unlike the coronavirus that caused the original SARS, this new one already possessed the ability to recognize a key protein in human cells named ACE2. “It had already found its best way of being a [human] virus,” he told The Atlantic.

‘This Virus is Slippery AF’

The post claims that a quick ability to mutate allowed the virus to mutate “in such a way the way [sic] that it causes great damage to human lungs” and that this fast mutation rate is “why Coronavirus is different from seasonal flu, or H1N1, or any other type of influenza.” The post asserts that the coronavirus, compared to other viruses, mutates unusually fast, i.e. that it is “slippery AF.” This is not true.

“The virus has been remarkably stable given how much transmission we’ve seen,” Lisa Gralinski, a professor of epidemiology at the University of North Carolina, said in the same Atlantic interview. “That makes sense,” she said, referring to its strong initial ability to infect human cells “because there’s no evolutionary pressure on the virus to transmit better. It’s doing a great job of spreading around the world right now.” David Ho, an epidemiologist at Columbia University’s Aaron Diamond AIDS Research Center, also made this point in a Q and A interview. “This virus is mutating but it has mutated very little so far,” he said.

“This virus does not seem to mutate any faster than we would expect,” Koci concurred. “It is mutating, all viruses do, and over time, the randomness of these mutations may spit out a new variant that is worse, but current rates of mutations do not seem unusual for these types of viruses.” Mutation rates also do not have anything to do with the damage COVID-19 causes to the lungs in some individuals, according to Ho. “There are differences [in various strains],” he said, “but probably they are functionally not important, so that’s not the explanation for why you see different disease courses among the infected,” he said.

The Mutation Rate Makes It Hard to Develop a Vaccine for COVID-19

The post accurately asserts that there are now two primary strains of the novel coronavirus, but inaccurately suggests this is unusual or a central problem in developing a vaccine for the virus:

It’s already mutated AGAIN, so that we now have two strains to deal with, strain S and strain L…which makes it twice as hard to develop a vaccine.

While multiple strains may complicate vaccine production efforts, it is unclear if the two present strains “are different enough that they would need separate vaccines or not,” Koci told us. More important, mutation rates and multiple strains would not be the reason for the potentially long time frame in the development of a coronavirus vaccine.

Influenza, as a comparison, mutates season to season, and epidemiologists are able to predict with varying degrees of accuracy which strains will spread each season thanks to a massive and international monitoring effort that collects data for this purpose. This information guides the production of flu shots for a given season.

“We do this for [the] flu, so we should be able to do it for this [novel coronavirus] too. The difference,” Koci told us, “is we’ve been studying [the] flu for almost 100 years. We have a pretty good idea of how we need to change the vaccine each year to keep pace.  It may take a while until we understand the differences in coronavirus strains at the same level, but we’ll get there.” Given the tools modern science has and the number of labs working on the problem world wide, Koci believes “we will catch up to where we are with our understanding of [the] flu pretty quick.

If It Mutates Again, Who Is to Say What It Will Do Next?

The post ends with a combination of good advice and misleading scare statements. The majority of the viral Facebook story is predicated on the false belief that the novel coronavirus mutates at a faster rate than other viral pathogens like influenza or even previous coronaviruses. There is no evidence to support that, in part because this novel coronavirus was, improbably, perfectly adapted to infect humans from the outset.

The fear, then, is not of an unknown about how mutations could change the disease to make it even more scary. Instead, the central fear expressed by many epidemiologists is that the public will not take the necessary precautions to slow its spread and, as a result, will overload the health system. That a large population of people will likely be infected with this disease in the coming year is likely, but how deadly that infection could be depends in large part on slowing the rate at which people develop new infections.

The reason for this is to create conditions that allow for these inevitable new cases to occur over a broader period of time, not all at once in a way that overloads the medical care system of a region. In the hard hit areas of northern Italy, the outbreak of new infections took place in a dangerously short period of time, necessitating hard decisions like denying ventilators to older patients less likely to survive. Staying at home is not only about preventing yourself from infection, it is, in most cases, primarily about preventing yourself from infecting multiple other individuals in a short period of time. In that light, the final point made in this viral post is a good one: “Stay home folks.”