elopment of a vaccine, Dr. Gale and his research team compared one strain from each of West Nile’s two basic categories: the harmful strains associated with outbreaks of encephalitis and meningitis in North America, and non-harmful strains from Madagascar and Cyprus.
They studied a harmful strain isolated from an infected grackle from Hall County, Texas, in 2002, and a harmless strain isolated from an infected parrot from Madagascar in 1978.
They mapped the genetic makeup of each strain, and then tested the viruses in mice.
West Nile infection triggers production of interferon, a group of proteins that are crucial in immune defense. Interferon, which binds to IFNAR, subsequently signals the JAK-STAT molecular pathway, a series of biochemical reactions essential for turning on immune-defense genes, allowing the body to clear out the virus. This process occurs normally in the African strain.
Infection by the Texas strain, however, blocked IFNAR signaling activity, allowing the virus to replicate and spread.
This highlights the integral role of interferon and IFNAR signaling in innate immunity.
Dr. Gale said the mechanisms at work in the African strain could be used as a basis for a vaccine, perhaps mutating North American strains so they no longer disrupt immune signaling. The remaining key is figuring out the exact mechanics of how the strains block signaling, a project Dr. Gale’s team is already at work on.
Fortunately, North American strains are extremely similar – in fact, the one that appeared in the United States in 1999 and the Texas strain used in this study are 99 percent identical. One vaccine could, in theory, prevent illness from many of the harmful strains, Dr. Gale said.
“We feel a vaccine could be highly effective in preventing infection,” said Dr. Gale.
Dr. Brenda Fredericksen of UT Southwestern and researchers from the Washington University School of MedicPage: 1 2 3 Related medicine news :1
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