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Letter
Virus Isolation and “Acute”
West Nile Virus Encephalitis (Response to Huang et al.)
Read original letter,
http://www.cdc.gov/ncidod/EID/vol8no12/02-0532.htm
Read Hindenburg's
reply, http://www.cdc.gov/ncidod/EID/vol9no5/03-0128.htm
Vijay K. Krishnamoorthy,* Jayashri Bhaskar,* and John N. Sheagren*
*Advocate Illinois Masonic Medical Center, Chicago, Illinois, USA
Suggested citation for this article: Krishnamoorthy
VK, Bhaskar J, Sheagren JN. Virus isolation and "acute" West
Nile virus encephalitis (response to Huang et al.). Emerg Infect Dis
[serial online] 2003 May [date cited]. Available from: URL: http://www.cdc.gov/ncidod/EID/vol9no5/03-0018.htm
To the Editor: We read with interest a recent article in your
journal, First Isolation of West Nile virus from a Patient with Encephalitis
in the United States (1); in the report, we were unable
to ascertain indisputable evidence that this patient had indeed acquired
acute West Nile virus (WNV) encephalitis. In animals (2,3)
and humans (4), West Nile virus can persist in the host
even after the host has recovered from an acute WNV infection, presumably
more so in the immunocompromised persons. Therefore, in the case described
by Huang et al. (1), proving that the patient did not
have a history of WNV infection is important, particularly because this
patient is from a geographic area where WNV is known to exist. The findings
at autopsy of perivascular lymphocyte cuffing in mammillary bodies of
the brain are not the classic findings reported during the West Nile encephalitis
outbreak in New York City (5). The immunoglobulin (Ig)
G antibody against WNV, if it had been present, would have been useful
in that IgG antibody in the absence of IgM antibody is indicative of past
rather than acute infection.
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.
References
- 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.
- 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.
- Camenga DL, Nathanson N, Cole GA. Cyclophosphamide-potentiated West
Nile viral encephalitis: relative influence of cellular and humoral
factors. J Infect Dis 1974;130:634–41.
- Southam CM, Moore AE. Induced virus infections in man by the Egypt
isolates of West Nile virus. Am J Trop Med Hyg 1954;3:19.
- Sampson BA, Armbrustmacher V. West
Nile encephalitis: the neuropathology of four fatalities. Ann N
Y Acad Sci 2001;951:172–8.
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