The findings, detailed in a report published online this week by the Proceedings of the National Academy of Sciences, come from studies of laboratory mice infected with the virus. It turns out that mice with a mutation in a gene encoding one of a group of enzymes known as oligoadenylate synthetases, which are known to help fight viral infections, die quickly from the disease. Wild mice carrying a normal copy of the gene, on the other hand, are almost completely resistant. The study results suggest that the enzyme plays a critical role in West Nile pathogenesis, conclude Jean-Louis Gunet of the Pasteur Institute in Paris and his colleagues.
The next step will be to scrutinize the same genetic region in humans. "Given the low background of immunity, [West Nile] virus spread and amplified transmission has the potential to result in future summertime epidemics," Charles Samuel of the University of California at Santa Barbara writes in an accompanying commentary. Understanding the role genes play in susceptibility and resistance, he adds, is thus of utmost importance.