Evolution is a natural process. In fact, the current form we occupy is due to natural evolution throughout many millenia. Although it might have taken millions of years for humans to evolve, this long biological time scale is not consistent across all types of organisms. This is painfully apparent with the rise of variants of the virus that causes COVID-19. In just one year we have seen the virus accumulate mutations in its genome that have the potential to contribute to its infecting power and pathogenicity.
These mutations are essentially random; every so often, this edit leads to a change in one of the viral proteins that allows the virus to evade detection by the immune system and reproduce much more than it could have without the mutation. Because this edited strain proliferates more effectively than other strains, it becomes dominant, and that is how we see a rise of infection with variants throughout the population.
Dami Collier and co-workers recently demonstrated the efficacy of antibodies elicited from the Pfizer-BioNTech vaccine against the B.1.17 variant of the coronavirus. To do this, they studied three cohorts of people (first dose, second dose, and previously infected with COVID-19) by infecting them with a pseudovirus that they engineered to have the mutations associated with the B.1.1.7 variant. After collecting and analyzing blood samples, they observed in all cohorts that there was a decrease in the abilities of the antibodies (whether from the vaccine or previous COVID-19 infection) to fight the virus; however, the group that received both doses of the vaccine showed the smallest loss in immunity. Collier and co-workers then performed a phylogenetic analysis—essentially constructing a family tree for all of the various coronavirus variants—and located a particularly pernicious mutation implicated in the virus’ escape from various antibodies in the B.1.1.7 lineage. Thus, they performed the aforementioned studies with a B.1.1.7 pseudovirus containing this mutation and observed a more severe loss of the individuals’ protection from the virus (Collier et al.).
To show mechanistically why this drop in protection might happen, the authors decided to probe how specific antibody isolates would perform in fighting these viral variants. When antibodies bind, they do not grab hold of the entire biomolecule (e.g., a protein), but instead, attach to very discrete domains. The authors decided to further investigate antibodies known to target specific domains of the spike protein, and if mutations in certain domains affected the binding affinity of these antibodies (and thus their ability to neutralize, or fight, the virus). Indeed, the authors showed that certain antibodies lost their ability to bind to specific domains of the spike protein that possessed these changes. However, the authors also showed that the mutations responsible for the virus’ escape from select antibodies also led to less binding of the spike protein to the receptor that allows the virus to enter human cells (Collier et al.).
While scientists must devise ways around the cunning of biology, the immunity provided from the vaccine is non-negligible and will further prevent the spread and inevitable mutation of the virus responsible for the COVID-19 pandemic.
Collier, D.A., De Marco, A., Ferreira, I.A.T.M. et al. "Sensitivity of SARS-CoV-2 B.1.1.7 to mRNA vaccine-elicited antibodies." Nature, vol. 593, no. 7857, 2021.
Last Fact Checked on May 25th, 2021.