Forget about the frenzy over COVID-19 variants, viral evolution is normal

There has been a media frenzy about SARS-CoV-2 variants in recent months, which is inciting panic and worry, and dissuading some persons from getting vaccinated due to concerns that the vaccines won’t be protective. News reports are feeding this frenzy with nearly daily updates citing every new unreviewed pre-print study on viral variants. Inflammatory overblown headlines scream at the public, like the Los Angeles Times Science section articles entitled “California’s coronavirus strain looks increasingly dangerous: ‘The devil is already here’” and “The ‘nightmare scenario’ for California’s coronavirus strain: Here is what we know.” There is a disappointing lack of perspective and balance; for example the above articles are based on interviews of a single source who is presenting his own yet unpublished work. There are many reasons to temper these messages and reassure the public regarding this alarmist deluge of dire predictions. 

COVID iral evolution 

Viral evolution is normal, and the implication that the virus is somehow directing itself to change in a sinister direction is at best a melodramatic misunderstanding of biology, and at worst misleading and misinforming the public as to why viruses change. Viruses have no will or intent; they adapt to their host just as water takes the shape of its container. In this case, SARS-CoV-2 has been in humans barely a year and is expected to change as it adapts to this new host. While it may become more contagious, there is no selective advantage to becoming more deadly; common cold coronaviruses that have circulated in humans for decades have diversified genetically but not become more harmful. In fact, viral evolution generally favors becoming less pathogenic, because survival of the host is obviously important for survival of the virus. Comparing a variant to “the devil” is both scientifically meaningless and inaccurate; what’s happening is entirely an expected natural process. 

COVID-19 vaccine on March 13, 2021, in Lynchburg, Virginia. (Photo: Andrew Caballero-Reynolds/AFP via Getty Images)

To date, predictions about the behavior of the virus have been almost entirely based upon laboratory tests of virus growing in cultured cells. The efficiency of virus spread between people is far more complex than virus spread in the laboratory, and it is unclear how laboratory tests predict what happens in the real world. Tests showing virus resistance to antibodies face similar caveats. Moreover, antibody resistance is not black and white; resistance depends on the amount of antibodies present and not absolute. Thus, a measurable change in susceptibility to antibodies may be insignificant compared to antibody levels in a person. Also, laboratory tests measure “neutralizing activity,” the ability of antibodies to interfere with viral growth directly, but that is only one function of antibodies, which have other antiviral mechanisms such as tagging viruses for destruction by immune cells that are not reflected in these experiments. Finally, the variants are not resistant to all antibodies; even if evolution alters SARS-CoV-2 enough that antibodies from vaccination lose efficacy, it will be a straightforward process to re-tool the existing RNA vaccines to elicit antibodies specifically against the new variants. 

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Surprisingly, the media and even most scientists are ignoring a key issue about how the immune system and the current vaccines work: antibodies are only one factor, perhaps even a minor component in determining the outcome of illness. Strong evidence from studies of treating patients with monoclonal antibodies or plasma antibodies indicates that they have little impact once someone has gotten seriously ill. It appears that antibodies are important only for preventing or slowing initial infection. After that, T cells (specifically killer T cells that destroy cells in our body containing abnormal proteins, such as viral proteins or cancer proteins) targeting virus-infected cells are pivotal in controlling and clearing infection. The current vaccines were designed to elicit both antibody and T cell responses, and the importance of the latter is suggested by the data that even when the vaccine fails to prevent infection, vaccinated persons are protected from severe illness. 

Mutations and vaccines

Mutations that affect neutralizing antibodies are extremely unlikely to affect such T cell responses. Neutralizing antibodies works by binding a small region of the viral spike protein that depends on a three-dimensional fitting interaction to bind, so it takes few mutations in spike to alter the shape of the antibody target to interfere. Killer T cells, on the other hand, target very short stretches of any region of viral proteins and typically target multiple areas; thus a few mutations will not interfere with the T cell response as a whole. It is highly unlikely that the few spike mutations in any of the variants known so far will affect the efficacy of T cell responses raised by vaccines. Thus, even if a variant were to escape the antibodies, the accompanying T cells should still prevent serious illness. 

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Finally, vaccines are only one tool in our public health repertoire and we should not be relying solely on them to return life “to normal.” All variants are still stoppable by masking, distancing, focused quarantining, and contact tracing. In some countries, these measures alone have been sufficient to entirely contain the pandemic, notably without prolonged business shutdowns. This success depends on getting ahead of the virus, and it is extremely unfortunate that some states are relaxing containment measures because infection rates are dropping. Indeed, now is the time to be doubling down on these measures because they are most effective when rates are low, and we could have the opportunity to stop widespread transmission altogether if we act aggressively now. 

Otto Yang is a professor of Medicine and associate chief of Infectious Diseases, David Geffen School of Medicine at University of California Los Angeles. 

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