In 1999 the now-infamous West Nile virus emerged in the eastern U.S., and every summer since then the scourge has resurfaced and spread. This year alone has witnessed 251 recorded cases, 11 of which resulted in death. Why certain of the virus's victims--around 20 percent--go on to develop symptoms while the others remain symptom-free has been a mystery. But new research suggests that some people infected with West Nile may carry a genetic mutation that predisposes them to developing the trademark fever and encephalitis.

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 Gu¿net 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.