DALLAS Oct. 3, 2006 -- West Nile virus evades the body's immune defenses by blocking immune signaling by a protein receptor, a finding that could pave the way for a vaccine to protect against North American strains of the virus, UT Southwestern Medical Center researchers report.
Researchers discovered the receptor's key role in controlling West Nile infection by conducting a study, described in October's Journal of Virology, that compares the genetics of an illness-causing Texas strain of the virus to a harmless African strain.
The Texas strain can inflict illness because it blocks the signaling activity of a protein receptor called the interferon alpha/beta receptor, or IFNAR, disrupting a cell's ability to direct the immune system to fight off the virus.
The African strain does not block IFNAR activity, so the immune system renders it harmless. The strain is harmful, however, in mice with dysfunctional receptors.
"We now hope to harness the African strain as the basis for West Nile vaccine studies. The virus has spread across the country and infected more than 2,100 U.S. residents 180 in Texas this year alone, so we have to learn how to deal with it," said Dr. Michael Gale, associate professor of microbiology at UT Southwestern and director of the study. Brian Keller, a student in the Medical Scientist Training Program at UT Southwestern, is the first author of the study.
West Nile virus, which is transmitted by mosquito bite, arrived in the United States in 1999 and has become an epidemic that flares up in the summer and lasts into fall.
Infection causes mild flu-like symptoms in most people, but about one in every 150 develop serious illness, that can include high fever, coma, seizures and encephalitis and meningitis. Children, the elderly or people with weak immune systems are most at risk.
There is no vaccine. Doctors can only treat symptoms of the disease.