Disease relevance of West Nile Virus

• Toll-like receptor 3 mediates West Nile virus entry into the brain causing lethal encephalitis [1].
• Analysis of the genome of the flavivirus responsible for the 1999 New York City encephalitis epidemic cloned from human brain by reverse-transcription polymerase chain reaction Indicates its identity as a lineage I West Nile virus (WNV; WNV-NY1999) closely related to WNVs previously isolated In the Middle East [2].
• Our results also reveal a novel cofactor-induced serpin mechanism of enzyme inhibition that could be explored for developing effective and selective inhibitors of other important induced fit viral proteases of the Flaviviridae family such as the West Nile virus NS3 endoprotease [3].
• Requirements for West Nile virus (-)- and (+)-strand subgenomic RNA synthesis in vitro by the viral RNA-dependent RNA polymerase expressed in Escherichia coli [4].
• Two strains of West Nile virus isolated from patient serum and brain-tissue samples reacted in hemagglutination-inhibition and neutralization tests with patients' convalescent-phase sera and immune ascites fluid from other strains of West Nile virus [5].

High impact information on West Nile Virus

• CCR5 deficiency increases risk of symptomatic West Nile virus infection [6].
• A large body of evidence suggests a critical role for the 1b isoform of the mouse Oas gene (Oas1b) in resistance to West Nile virus (WNV) infection in vivo [7].
• A previous study has illustrated that the alphaVbeta3 integrin served as the functional receptor for West Nile virus (WNV) entry into cells [8].
• The 2',5'-oligoadenylate synthetase 1b is a potent inhibitor of West Nile virus replication inside infected cells [7].
• Interaction of West Nile virus with alpha v beta 3 integrin mediates virus entry into cells [9].

Chemical compound and disease context of West Nile Virus

• From the Centers for Disease Control and Prevention. West Nile Virus activity--United States, 2001 [10].
• In this study, we purified a recombinant, secreted form of West Nile virus (WNV) NS1 glycoprotein from baculovirus-infected insect cells and generated 22 new NS1-specific monoclonal antibodies (MAbs) [11].
• Outbreak of West Nile virus infection, Volgograd Region, Russia, 1999 [12].
• Correspondingly, castanospermine had no adverse or protective effect on West Nile virus mortality in an analogous mouse model [13].
• [3H]uridine-labeled extracellular West Nile virus (WNV) particles produced by cell cultures obtained from genetically resistant C3H/RV and congenic susceptible C3H/HE mice were compared by sucrose density gradient centrifugation as well as by analysis of the particle RNA [14].

Biological context of West Nile Virus

• Major histocompatibility complex class I (MHC-I) induction by West Nile virus: involvement of 2 signaling pathways in MHC-I up-regulation [15].
• BACKGROUND: Between August 25 and September 25, 2003 seven patients with West Nile virus neurological manifestations were identified through the hospital neurology consultation services in Calgary, Alberta, Canada. Three of the seven patients were treated with interferon alpha-2b (IFN alpha-2b) [16].

Anatomical context of West Nile Virus

• CD8+ T cells require perforin to clear West Nile virus from infected neurons [17].
• Expression of E-selectin (ELAM-1, CD62E) on human umbilical vein endothelial cells significantly increased 30 min postinfection with the flavivirus West Nile virus (WNV), was maximal by 2 h postinfection, and declined to baseline levels within 24 h [18].
• Vero cells were infected by Kunjin virus and radiolabelled in the presence of the leucine analogue, threo-beta-hydroxy-DL-leucine (THL) [19].
• Characterization of a 105-kDa plasma membrane associated glycoprotein that is involved in West Nile virus binding and infection [20].

Gene context of West Nile Virus

• Inhibition of interferon signaling by the New York 99 strain and Kunjin subtype of West Nile virus involves blockage of STAT1 and STAT2 activation by nonstructural proteins [21].
• Different chemokine expression in lethal and non-lethal murine West Nile virus infection [22].
• West Nile virus evades activation of interferon regulatory factor 3 through RIG-I-dependent and -independent pathways without antagonizing host defense signaling [23].
• West Nile virus discriminates between DC-SIGN and DC-SIGNR for cellular attachment and infection [24].
• The Src family kinase c-Yes is required for maturation of West Nile virus particles [25].

Analytical, diagnostic and therapeutic context of West Nile Virus

• Peptide mapping of [3H]leucine-labelled gp66, gp54 and the envelope glycoprotein E of West Nile virus demonstrated that gp66 and gp54 were related to E, and that the peptides of gp54 were a subset of those of gp66 [26].
• Detection of West Nile virus using formalin fixed paraffin embedded tissues in crows and horses: quantification of viral transcripts by real-time RT-PCR [27].
• The third vaccination trial was based on West Nile virus (WNV) harvested from infant mouse brain, inactivated with formalin and oil adjuvanted [28].
• Passive immunization with rabbit anti-E protein sera also partially protected mice from challenge with West Nile virus [29].
• Enzyme immunoassay testing of the sera indicated that the prevalence of antibody was 9% (21/223) for Sicilian sandfly fever, 4% (8/223) for Rift Valley fever, 3% (15/437) for West Nile virus and 9% (28/315) for Hantaan (HTN) virus [30].

References