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West Nile Virus Epidemic Expands, Even by Transplant Organs, Blood

Nick Leggio of New Orleans holds a dead blue jay as he waits for the bird to be picked up for testing for West Nile virus. (AP Photo/Cheryl Gerber.)

This year West Nile (WN) virus made it as far west as Colorado traveling in birds and insects, and clear across the United States to California in humans—a scant three years after it first appeared in New York City. By mid-September more than 2,700 people became sick with this infection, and close to 150 have died. And this expansion appears far from being finished.

"There is a massive increase in West Nile virus activity this year compared to previous years, over a wider geographic area," says Lyle Peterson, a WN virus expert at the Centers for Disease Control and Prevention (CDC) in Atlanta, Ga. "Its size and scope are remarkable."

Several of the warm and humid southern states, with more mosquitoes and a longer mosquito season than the rest of the United States, were especially hard hit. Midwestern states such as Illinois and Michigan also suffered unusually high case loads. "It could be a combination of things," says John Roehrig, chief of the CDC arbovirus diseases branch of the Illinois caseload. "They did have WN virus activity last year, but its difficult to speculate. In the 1975 St. Louis encephalitis outbreak, Chicago was fairly heavily involved."

Transmission of the virus by mosquitoes accounts for the overwhelming majority of WN cases, but recipients of transplanted organs and blood are also becoming infected when the virus hitchhikes its way within those donated tissues.

In studying the epidemic, scientists are trying to learn why some people infected with WN virus quickly become gravely ill, while others experience few or no symptoms. Recent mouse studies conducted separately by researchers at the Institut Pasteur in Paris, France, and also at Georgia State University and the Georgia Institute of Technology in Atlanta provide clues suggesting that a variant gene might be responsible for some of these differences in susceptibility.

The investigators identified a "specific gene" that is involved in the natural defense of mice against WN virus infection, according to Catherine Laughlin, chief of the virology branch in the division of microbiology and infectious diseases at the National Institute of Allergy and Infectious Diseases in Bethesda, Md. That gene, which encodes 2’,5’-oligoadenylate synthetase 1 (OAS) 1b, plays a role in "interferon-induced activation of RNAse L leading to degradation of viral and cellular RNAs," she says. Although the mechanism behind this mouse resistance to WN virus is far from certain, she adds, "once the mechanism is understood, it should be possible to design synthetic therapeutic agents that provide the same protection as the natural possession of a complete OAS 1b gene."

CDC's Peterson offers a cautionary note. "Nobody knows if humans have a genetic susceptibility to severe [WN] infection," he says, noting that these results from experiments involving mice might not apply to humans. "The overwhelming risk factor for severe disease [in humans] is age," he points out.

Meanwhile, the WN virus does not appear to be changing in any way in terms of host range as it continues to move westward, according to Roehrig from CDC. "Since 1999, there have been at least 115 bird species shown to be infectable with WN virus," he says. "As the virus moves west and encounters different birds, it's likely that other species will be added to this list." Moreover, the virus appears to be genetically stable since 1999, although "there is no gene sequence information available in 2002, but those studies are planned." Because arboviruses replicate in many different animal species, "they are quite genetically stable," he says.

Experts believe that infection with the WN virus is likely to confer lifelong immunity. "We don't know that for sure, but data on related viruses and epidemiology of WN virus in highly endemic areas suggests this is the case," Peterson says. "Higher levels of immunity would make less people and birds susceptible for infection. This would tend to decrease the likelihood of an epidemic." Prospects for a vaccine are uncertain. There is an inactivated vaccine for horses that is experimental, but available commercially. No vaccine exists for humans. "Several groups are working on vaccine development, but a vaccine for humans is years away," he says.

In related developments, the CDC assigned an additional nearly $20 million to states for WN virus activities as a result of the increase in cases, bringing the total federal funding to states for WN virus this year to $35 million. Also, the Food and Drug Administration approved the first field test of the drug interferon to treat WN infection. Intron A, made by Schering-Plough, is used to treat hepatitis B and C, and has shown some efficacy against West Nile in lab tests. Hepatitis C virus, like WN, is a flavivirus, although the two are not closely related. However, an uncontrolled, open-label trial of interferon in patients with St. Louis encephalitis, which is closely related to WN virus, suggested it might have a beneficial effect.

Marlene Cimons
Marlene Cimons is a freelance writer in Bethesda, Md.