These results indicate that patients co-infected with HCV and HIV-1 can mount immunoglobulin and CTL responses directed against HCV F protein that are fully comparable in scope and magnitude with those observed in individuals infected with HCV alone.
Hepatitis 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.To characterize the evolution of hepatitis C virus (HCV) disease and the influence of human immunodeficiency virus type 1 (HIV-1) and antiretroviral therapy (ART) (17), longitudinal sequence analysis of E2 envelope gene hypervariable region 1 (HVR1) was undertaken for two male Caucasian children (C1 and C2), who acquired HCV and HIV-1 infection by mother-to-child transmission.Patient C1, born in 1996, was treated from birth with zidovudine, which was complemented with lamivudine when HIV-1 cocultures became positive at 6 weeks of age. Early HIV-1 viremia correlated with a rise in CD8 cell counts, a sharp decline in CD4 counts, and an inversion of the CD4:CD8 ratio, consistent with acute HIV-1 infection ( Fig. 1A and B) (3). HIV-1 viral load decreased and stabilized at the end of the first year of life, while CD4 counts remained within the normal range. At 1.16 years of age, combination ART (lamivudinestavudine-ritonavir) was introduced, resulting in a further decline in HIV-1 viral load and a rise in CD4 counts (Fig. 1). Levels of alanine (ALT) and aspartate (AST) aminotransferases peaked 36 days later, followed by a decline over the following weeks without a change in treatment (Fig. 1C). Infection with HCV-1b (21) at 1.77 years of age was confirmed by PCR. Stored plasma samples were used retrospectively to measure HCV RNA levels, which were not influenced by ART (Fig. 1B). Between the ages of 3 and 6, HIV-1 levels declined but remained detectable, HCV viral load was stable, ALT and AST levels remained at twice normal or less, and CD4 counts declined but remained within the normal range ( Fig. 1) (3). A liver biopsy performed at 5.83 years of age showed chronic hepatitis characterized by distorted lobular architecture together with mild, diffuse lobular inflammation with occasional nodular lymphoid infiltrate and prominent macro-and microvesicular steatosis. Portal tracts were expanded with mononuclear cell infiltrates, and interface hepatitis was present in the majority. Mild periportal and sinusoidal fibrosis was observed.At 4.5 months later, changes in ART brought the HIV-1 viral load to Ͻ50 copies/ml and raised CD4 counts. Common clinical complications related to pediatric HIV infection were not seen. HCV RNA was extracted from plasma and was amplified using previously described primers and conditions (8,9). Strict PCR precautions were adopted. A total of 115 independent subclones were sequenced. Multiple alignments were performed using Clustal X version 1.81 (30). Overall, accumulation of nucleotide substitutions was observed within HVR1 (nucleotides 1482 to 1562), while f...
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