CCR5 limits cortical viral loads during West Nile virus infection of the central nervous system.

Background: Cell-mediated immunity is critical for clearance of central nervous system (CNS) infection with the encephalitic flavivirus, West Nile virus (WNV). Prior studies from our laboratory have shown that WNV-infected neurons express chemoattractants that mediate recruitment of antiviral leukocytes into the CNS. Although the chemokine receptor, CCR5, has been shown to play an important role in CNS host defense during WNV infection, regional effects of its activity within the infected brain have not been defined.

Identification of the authentic varicella-zoster virus gB (gene 31) initiating methionine overlapping the 3' end of gene 30.

The varicella-zoster virus (VZV) gB sequence was re-examined in light of recent knowledge about unusually long gB signal peptides in other herpesviral gB homologs. Through mutational analysis, the discovery was made that the authentic initiating methionine for VZV gB is a codon beginning at genome nucleotide 56,819. The total length for the VZV gB primary translation product was 931 amino acids (aa) with a 71-aa signal sequence.