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Date: Dec 10, 2002
Posted by: ERAP (envrisk@cornell.edu)

At least 5 research articles in the current issue of the CDC journal Emerging Infectious Diseases 8 (12. December 2002 ) focus on West Nile Virus. All can be accessed online from http://www.cdc.gov/ncidod/EID/index.htm. Synopses of these articles follow:

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First Isolation of West Nile virus from a Patient with Encephalitis in the United States
http://www.cdc.gov/ncidod/EID/vol8no12/02-0532.htm
Cinnia Huang* et al. ( *Wadsworth Center, New York State Department of Health, Albany, New York, USA)

Abstract: West Nile virus (WNV) was isolated from a patient who developed encephalitis while undergoing treatment with CHOP (cyclophosphamide, hydroxydoxorubicin, vincristine [Oncovin], predisone) and rituximab for a non-Hodgkin B-cell lymphoma. Both standard reverse transcription-polymerase chain reaction (RT-PCR) and Taqman RT-PCR established the diagnosis of WNV infection from cerebrospinal fluid (CSF). Several whole blood samples and one serum sample underwent further testing. CSF and serum samples were negative for WNV antibody; however, all samples were positive by both RT-PCR assays. Infectious virus was recovered from a blood sample, and its identity was confirmed by using a WNV-specific immunofluorescence assay. The complete WNV genomes determined from CSF and from the virus isolate adapted from cell culture were the same. The results represent the first complete WNV genome sequence obtained directly from human CSF and the first time that infectious WNV has been recovered from a patient with encephalitis in North America.

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Vector Competence of California Mosquitoes for West Nile virus
http://www.cdc.gov/ncidod/EID/vol8no12/02-0536.htm
Laura B. Goddard* et al. (*University of California, Davis, California, USA)

Abstract: To identify the mosquito species competent for West Nile virus (WNV) transmission, we evaluated 10 California species that are known vectors of other arboviruses or major pests: Culex tarsalis, Cx. pipiens pipiens, Cx. p. quinquefasciatus, Cx. stigmatosoma, Cx. erythrothorax, Ochlerotatus dorsalis, Oc. melanimon, Oc. sierrensis, Aedes vexans, and Culiseta inornata. All 10 became infected and were able to transmit WNV at some level. Ochlerotatus, Culiseta, and Aedes were low to moderately efficient vectors. They feed primarily on mammals and could play a secondary role in transmission. Oc. sierrensis, a major pest species, and Cx. p. quinquefasciatus from southern California were the least efficient laboratory vectors. Cx. tarsalis, Cx. stigmatosoma, Cx. erythrothorax, and other populations of Cx. pipiens complex were the most efficient laboratory vectors. Culex species are likely to play the primary role in the enzootic maintenance and transmission of WNV in California

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Efficacy of Killed Virus Vaccine, Live Attenuated Chimeric Virus Vaccine, and Passive Immunization for Prevention of West Nile virus Encephalitis in Hamster Model
http://www.cdc.gov/ncidod/EID/vol8no12/02-0229.htm
Robert B. Tesh* et al (*University of Texas Medical Branch, Galveston, Texas, USA; and  Acambis, Inc.)

Abstract: Results of experiments evaluating the efficacy of three immunization strategies for the prevention of West Nile virus (WNV) encephalitis are reported. Immunization strategies evaluated included a killed virus veterinary vaccine, a live attenuated chimeric virus vaccine candidate, and passive immunization with WNV-immune serum; all were tested by using a hamster model of the disease. Each product protected the animals from clinical illness and death when challenged with a hamster-virulent wild-type WNV strain 1 month after initial immunization. The live attenuated chimeric virus vaccine candidate induced the highest humoral antibody responses, as measured by hemagglutination inhibition, complement fixation, and plaque reduction neutralization tests. Although the duration of protective immunity was not determined in this study, our preliminary results and the cumulative experience of other virus vaccines suggest that the live attenuated chimeric virus provides the longest lasting immunity.

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Induction of Inflammation by West Nile virus Capsid through the Caspase-9 Apoptotic Pathway
http://www.cdc.gov/ncidod/EID/vol8no12/02-0224.htm
Joo-Sung Yang* et al (*University of Pennsylvania, Philadelphia, PA, USA; and  Viral Genomix, Inc.)

Abstract: West Nile virus (WNV) is a member of the Flaviviridae family of vector-borne pathogens. Clinical signs of WNV infection include neurologic symptoms, limb weakness, and encephalitis, which can result in paralysis or death. We report that the WNV-capsid by itself induces rapid nuclear condensation and cell death in tissue culture. Apoptosis is induced through the mitochondrial pathway resulting in caspase-9 activation and downstream caspase-3 activation. Capsid gene delivery into the striatum of mouse brain or interskeletal muscle resulted in cell death and inflammation, likely through capsid-induced apoptosis in vivo. These studies demonstrate that the capsid protein of WNV may be responsible for aspects of viral pathogenesis through induction of the apoptotic cascade.

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West Nile virus Epidemic in Horses, Tuscany Region, Italy
http://www.cdc.gov/ncidod/EID/vol8no12/02-0234.htm
Gian Luca Autorino* et al. (*Istituto Zooprofilattico Sperimentale delle Regioni Lazio e Toscana, Rome, Italy

Abstract: During the late summer of 1998, veterinary authorities in Tuscany, Italy, received reports of cases of neurologic disease among horses residing in a large wetland area located in the provinces of Florence and Pistoia. West Nile virus was isolated from two of the six horses that died or were euthanized. A retrospective epidemiologic study identified 14 clinical neurologic cases that occurred from August 20 to October 6 (attack rate of 2.8%). A serologic survey conducted over a 700-km2 area in stables with and without apparent clinical cases confirmed a wider spread of the infection, with an overall seroprevalence rate of 38% in the affected area. No significant differences in age-specific prevalence were observed, suggesting that the horses residing in the area had not been exposed previously to West Nile virus and supporting the hypothesis of its introduction in the wetland area during the first half of 1998.

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