The CDC says the Pfizer vaccine’s efficacy reduced from 91% to only 66% effective against the Delta variant. While the delta variant continues to account for the vast majority of cases in the United States, some researchers believe that the lambda and mu variants may weaken vaccine protection against both symptomatic and asymptomatic infection.
Mrs. Mallela, a pharmaceutical scientist and structural biologist at the University of Colorado Anschutz Medical Campus who has investigated how mutations affect COVID-19 vaccines and therapies, says it’s still unknown when current vaccine formulae will no longer function against certain variants. “At this time, the main goal is to figure out how long these vaccines developed against the wild-type virus will work against the next variant,” Mallela says. “Can we predict the next variant?” is another way of expressing it.
The existing vaccines still provide good protection against serious illness and death, but their advantages are dwindling, prompting requests for booster shots and other measures to reduce transmission. And there’s a chance that a completely vaccine-resistant variant will emerge: Pfizer CEO Albert Bourla warned last month that his company is preparing for such a scenario.
It’s critical to consider how viruses evolve to understand how we got here (and what might happen next).
SARS-CoV-2 virus mutations occur every 11 to 15 days on average. They can be caused by a variety of factors, including RNA replication mistakes.
Viruses evolve to prefer characteristics that aid in their survival, similar to how certain traits from ancient humans, such as bipedal walking and opposable thumbs, have been handed down to much of today’s population. While the majority of mutations have no effect on the virus’ general structure, the few that do can result in variants that evade antibodies created by vaccines or natural infections, as well as monoclonal antibodies and convalescent plasma therapy.
These life-saving techniques, unfortunately, can contribute to the creation of variants. According to Vaibhav Upadhyay, a postdoctoral fellow at the University of Colorado Anschutz Medical Campus and co-author on Mallela’s new article, once people receive treatments and vaccines with insufficient efficacy, SARS-CoV-2 seizes the opportunity to expand within them. After all, breaking into a house with a shoddy security system is significantly easier.
Although the relationship between infectiousness, illness severity, and antibody evasion isn’t fully obvious, mutations can make the virus more infectious. While the beta variant has thus far proven to be the most resistant to immunization, delta is anticipated to be significantly more contagious. Scientists like Guowei Wei of Michigan State University have projected current infectivity and antibody breakthrough rates, but it’s still unclear which variants make individuals worse.
Wei and other researchers are analyzing the precise regions in the virus’s genome where these mutations are taking place, particularly those that could improve infectivity and antibody evasion, in order to better understand the virus’s uncertain future. Most COVID-19 vaccines and antibody therapies target the virus’s spike protein receptor-binding domain (often referred to as RBD). This is due to the fact that the spike protein is an important component of the infection process: The virus links its spike protein to the human ACE2 enzyme on a human cell’s surface and “unlocks” it, allowing it to enter. Cells in the nose and throat are the first to be affected.
However, as Mallela and colleagues reveal in a new Journal of Biological Chemistry publication, variants appear to be tinkering with the protein structure in order to strongly connect with ACE2 and escape neutralizing antibodies.
Other RNA viruses, such as HIV and influenza, evolve more swiftly than SARS-CoV-2, despite all the unknowns. However, given the scarcity of well-proven treatments and the fading vaccine of vaccines, its progression is alarming. Our immune system and the virus are playing a cat-and-mouse game, according to Mallela.
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