Perez found that one of the two of the genetic mutations in his lab strain that enabled respiratory transmission between mammals was on the tip of the HA surface protein, one of the sites where human antibodies created in response to current vaccines would bind.
"Because the binding site of the mutant virus is different from the virus upon which the vaccine is modeled, it may mean that current vaccine stocks would not be as effective against the H9N2 mutant strain as previously anticipated," said Perez. "We should keep this in mind when designing vaccines for an avian flu pandemic in humans."
However, scientists cannot predict what the actual mutations will look like if and when they occur in nature, or even which strain of avian influenza will mutate to infect mammals.
"This is just the tip of the iceberg," said Perez. "Many more studies have to be done to see which combinations of mutations cause this type of transmission before we can design the appropriate vaccines."
Perez will be talking this week with the NIH and the CDC to discuss his team's role in researching the current swine flu virus strain. Perez will likely do studies related to vaccine development, virus transmission between humans and animals, and the pathogenesis of the virus.
A virus vaccine is derived from the virus itself. The vaccine consists of virus components or killed viruses that mimic the presence of the virus without causing disease. These prime the body's immune system to recognize and fight against the virus. The immune system produces antibodies against the vaccine that remain in the system until they are needed. If that virus, or in some cases a closely similar one is later introduced into the system,
|Contact: Lee Tune|
University of Maryland