MONDAY, Aug. 19, 2002 (HealthDayNews) -- Scientists in France have completed research that could help explain why only a fraction of those infected with West Nile virus become seriously ill.
The mosquito-borne virus has caused 11 deaths and 147 illnesses across the United States so far this year in what experts are calling the worst outbreak in the nation's history.
Most of those who are infected by West Nile through a mosquite bite will never know they were hit. Some, though, will develop flu-like symptoms and an even smaller number, usually the elderly and those with compromised immune symptoms, will develop potentially fatal encephalitis.
A similar dynamic has been observed in mice: The virus causes encephalitis and death in most lab rats, but IT doesn't affect wild mice at all, something which led scientists to believe there may be a genetic component at work.
The percentage of people who become severely ill depends on the particular strain of the virus, the researchers say.
In a new study, reported in this week's Proceedings of the National Academy of Sciences, the researchers used a strain previously found in Israel and the United States that had caused about 20 percent of infected people to become seriously ill.
The researchers, based at Institut Pasteur in Paris, injected mice with a highly virulent strain of West Nile isolated from an infected stork found in Israel in 1998. They then compared genetic markers in wild mice with the same markers in lab mice and found that a particular group of genes called oligoadenylate synthetases (OAS), which are normally involved in fighting viral infections, had mutated in the susceptible mice.
"So far, this is only a correlation but still, it is absolute," say Jean Louis Gunet and Philippe Desprs, who co-authored the study. The researchers have not found the same genetic features in resistant mice.
Is the same thing at work in humans?
"The putative significance of this is that this mutation appears to impair the functional immune response in the mouse, so in essence what you're talking about is getting to the same endpoint by two different routes," says Dr. Don Krogstad, Henderson professor of tropical medicine and director of the center for infectious disease at Tulane University in New Orleans.
"The common denominator is immunosuppression, and the message is that you can reach that level of impaired function by several routes, some of which are genetic and some of which are acquired. So, in that sense, it takes away the chasm between the heredity and the nature/nurture argument," he adds.
Krogstad does not rule out the possibility that a similar mutation will be found in humans. "It is conceivable in humans, but not yet demonstrated," he says.
The study authors appear to be more confident on that point.
"Even if the organization of the OAS cluster of genes is not exactly the same in humans and in mice, the same innate mechanism of defense exists in both species," Gunet and Desprs say.
"It is absolutely true that immunodepressed people are more susceptible than normal, healthy people. But this is trivial!" the authors write. "They are susceptible to many other diseases as well. We believe that the same mutation, should it exist in the human, should also lead to an extreme susceptibility."
What To Do
For more information on West Nile virus, how it's spread and how you can protect yourself, visit Fight the Bite Louisiana or the Centers for Disease
Control and Prevention.
