Monoclonal antibodies directed against hepatitis C virus (HCV) E2 protein can neutralize cell-cultured HCV and pseudoparticles expressing envelopes derived from multiple HCV subtypes. For example, based on antibody blocking experiments and alanine scanning mutagenesis, it was proposed that the AR3B monoclonal antibody recognized a discontinuous conformational epitope comprised of amino acid residues 396-424, 436-447, and 523-540 of HCV E2 envelope protein. Intriguingly, one of these segments (436-447) overlapped with hypervariable region 3 (HVR3), a domain that exhibited significant intrahost and interhost genetic diversity.
View Article and Find Full Text PDFA large share of hepatitis C virus amino acid sequence variation is concentrated within two hypervariable regions located at the N-terminus of the E2 envelope glycoprotein (HVR1 and HVR2). Interhost and intrahost comparison of 391 E2 sequences derived from 17 subjects infected with HCV using amino acid entropy revealed clustering of amino acid variability at a third site (residues 431-466), which was termed HVR3. Genetic distance analysis supported the division of HVR3 into three subdomains (HVR3a, HVR3b, and HVR3c).
View Article and Find Full Text PDFBackground: Hepatitis C virus (HCV) F protein is encoded in an alternate reading frame overlapping the core protein region. Its precise sequence, biological function and mode of expression are currently unclear. This study was conducted to examine the prevalence and characteristics of host humoral and cell-mediated immune responses directed against F protein in patients co-infected with HCV and HIV-1.
View Article and Find Full Text PDFHepatitis C virus (HCV) quasispeciation was studied in two children vertically coinfected with HCV and human immunodeficiency virus type 1 (HIV-1). HCV quasispecies diversification and liver injury were more significant in patient C1, who was immunocompetent with anti-HIV therapy, than in patient C2, who was immunosuppressed, in consistency with modulation of HCV quasispeciation and liver injury by immunocompetence in coinfected children.
View Article and Find Full Text PDF