![]() ![]() Also, newly formed viruses must detach from infected cells before they can spread to the next uninfected cell. "Excessively sticky viruses may end up binding to cells lining the nose or throat or to blood cells and may not make it into lung cells. "The virus must strike the right balance, however," Dr. Yewdell, the virus can shield its hemagglutinin antigenic sites from antibody attack by binding more tightly to its receptor. In contrast, the hemagglutinin gene in 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. Sequencing revealed that the unvaccinated mice - which lacked vaccine-induced antibodies - had no mutated influenza viruses in their lungs. "Now, with automated gene sequencers, sequencing of dozens of isolates is easily done overnight," he says. Yewdell, gene sequencing was not possible in the mid-1950s, when the nature of the gene was first elucidated, and until very recently, sequencing was expensive and time-consuming. After the final passage, the researchers sequenced the gene encoding the virus hemagglutinin protein. Some mice were first vaccinated against this virus strain and developed antibodies against it, while others were unvaccinated.Īfter infecting the vaccinated and unvaccinated mice with the 1934 influenza strain, the scientists isolated virus from the lungs of both sets of mice and passed on these viruses to a new set of mice. The team infected mice with a strain of seasonal influenza virus that had circulated in Puerto Rico in 1934. ![]() So he and his colleagues turned to a classic mouse model system developed in the mid-1950s at the University of Chicago, but used rarely since. It is not possible to dissect the mechanism of antigenic drift in people directly, notes Dr. These mutant viruses survive, multiply and are passed to person B, where the process is repeated. Mutant viruses that arise in person A can escape antibodies by replacing one critical amino acid in this antigen region. Antibodies in person A, for example, may mount an attack in which antibodies focus on a single antigenic region. With varying success, antibodies recognize one or more of the four antigenic regions in hemagglutinin, the major outer coat protein of the flu virus. According to the prevailing theory, drift occurs as the virus is passed from person to person and is exposed to differing antibody attacks at each stop. ![]() "No one is sure exactly how the antigenic drift of flu viruses happens in people," says Dr. "This research elegantly combines modern genetic techniques with decades-old approaches to give us new insights into the mechanisms of antigenic drift and how influenza viruses elude the immune system," says NIAID Director Anthony S. Bennink, Ph.D., led the research team, whose findings appear in the current issue of Science. The findings in mice, using a strain of seasonal influenza virus first isolated in 1934, also suggest that antigenic drift might be slowed by increasing the number of children vaccinated against influenza. Now, researchers from the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health, have proposed a new explanation for the evolutionary forces that drive antigenic drift. 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. Influenza viruses evade infection-fighting antibodies by constantly changing the shape of their major surface protein. National Institute of Allergy and Infectious Diseases (NIAID) Each year’s flu vaccine contains three flu strains-two A strains and one B strain-that can change from year to year. ![]()
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |