Virus isolation and "acute" West Nile virus Encephalitis (response to Huang et al.). (Letters).
The WNV copy numbers in clinical samples and clinical indices (leukocyte count) suggest that the virus multiplies in the setting of leukopoenia or immune suppression and cannot be definitive proof that it was an acute infection, unless a negative preillness sample was available. The cause of the transient viremia, whether acutely acquired or from increased proliferation in a chronic infection, needs to be clarified further. In the future, antigen detection will guide patient management decisions; therefore, the possibility of a human chronic carrier state warrants study.
(1.) Huang C, Slater B, Rudd R, Parchuri N, Hull R, Dupuis M, et al. First isolation of West Nile virus from a patient with encephalitis in the United States. Emerg Infect Dis 2002;8:1367-71.
(2.) Pogodina VV, Frolova MP, Malenko GV, Fokina GI, Koreshkova GV, Kiseleva LL, et al. Study on West Nile virus persistence in monkeys. Arch Virol 1983;75:71-86.
(3.) Camenga DL, Nathanson N, Cole GA. Cyclophosphamide-potentiated West Nile viral encephalitis: relative influence of cellular and humoral of four fatalities. Ann N Y Acad Sci 2001;951:172-8.
Address for correspondence: Vijay Kumar Krishnamoorthy, Department of Internal Medicine, Advocate Illinois Masonic Medical Center, 836 West Wellington Street, Chicago, IL 60657, USA; fax: 773-296-5361; email: Vijay.Krishnamoorthy-MD@advocate health.com
Vijay K. Krishnamoorthy, * Jayashri Bhaskar, * John N. Sheagren *
* Advocate Illinois Masonic Medical Center, Chicago, Illinois, USA
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|Author:||Sheagren, John N.|
|Publication:||Emerging Infectious Diseases|
|Article Type:||Brief Article|
|Date:||May 1, 2003|
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