The development of SARS-CoV-2 variants isn’t a surprise. The shocking thing, based on what we thought we knew about coronaviruses, is the speed at which variants developed and spread. The question remains: Should we be worried?

All things that multiply by copying their genetic code, including humans, make mistakes from time to time. In other words, all of the copies of the genetic code may not be identical to the original. These mistakes or changes in the code are known as mutations.

Unlike the superpower-conferring mutations in movies, most mistakes are either neutral or harm the health of the organism. The mutations that improve the ability of the virus to spread from person to person become more common over time. Variants differ from the original virus by containing one or more of these mutations that help the virus spread.

When it comes to human health, the variants aren’t necessarily bad. Some variants are less likely to make people ill. The benefit to the virus is that the infected person is less likely to be lying in bed sick and is out and about, spreading the virus to others.

The outbreak of the original SARS-CoV-1 in 2003 was much easier to control because it made people so sick shortly after infection that most were hospitalized. Ill people were much easier to recognize, isolate from others and made contact tracing easier. On the other hand, some variants may cause worse illness.

The biggest problem is that variants can make COVID-19 tests inaccurate, render monoclonal antibody treatments less useful and reduce vaccine effectiveness. Fortunately, the effectiveness of the mRNA vaccines (Pfizer and Moderna) against current variants appears to be unaffected or only mildly reduced. The picture may not be as bright for the AstraZeneca and Johnson & Johnson vaccines when it comes to the South African variant. Time will tell.

There are two theories as to why the variants developed so quickly. The first is that the tremendous number of infections around the world made for a huge number of chances for mutations to occur. Remember, there is a chance of mutation each time the virus replicates.

The second theory holds that the virus multiplies for long periods in people with suppressed immune systems, allowing it to mutate and adapt. Such people may have suppressed immune systems because of anti-rejection drugs following organ transplantation or during chemotherapy for cancer treatments. A small number of studied immunosuppressed individuals that fought COVID-19 for months have been found to develop new viral mutations. Still, there is no evidence that the mutated viruses spread to others.

We can slow the development of variants by decreasing the number of SARS-CoV-2 infections. Masks and social distancing help. Vaccination remains the best option.

The good news is the current vaccines can be rapidly changed to address the variants. Similar to the flu vaccine, we may have an annual COVID-19 vaccine that contains one or more of the circulating variants. Studies are under way.

Vaccine Smarts is written by Sealy Institute for Vaccine Sciences faculty members Drs. Megan Berman, an associate professor of internal medicine, and Richard Rupp, a professor of pediatrics at the University of Texas Medical Branch. For questions about vaccines, email vaccine.smarts@utmb.edu.

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