BETHESDA, Md., Oct. 30 (UPI) -- U.S. researchers propose a new explanation for the evolutionary forces that drive antigenic drift, a process that changes the characteristics of a virus.
Researchers from the National Institute of Allergy and Infectious Diseases, part of the National Institutes of Health, said influenza viruses evade infection-fighting antibodies by constantly changing the shape of their major surface protein.
This shape-shifting -- called antigenic drift -- is why influenza vaccines, which are designed to elicit antibodies matched to each year's circulating virus strains, must be reformulated annually.
Dr. Jonathan Yewdell said the prevailing theory is that the drift occurs as the virus is passed from person to person and is exposed to differing antibody attacks at each stop.
The researchers' study, using gene sequencing, revealed that unvaccinated mice, which lacked vaccine-induced antibodies, had no mutated influenza viruses in their lungs. In contrast, the hemagglutinin gene -- responsible for binding the virus to the cell that is being infected -- in a virus isolated from vaccinated mice had mutated in a way that increased the ability of the virus to adhere to the receptors it uses to enter lung cells.
The study, published in Science, found that decreasing the number of people not exposed to influenza -- by increasing the number of children vaccinated against influenza -- could slow the rate of antigenic drift and extend the duration of effectiveness of seasonal influenza vaccines.
