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Background.Inflammation persists in treated human immunodeficiency virus (HIV) infection and may contribute to an increased risk for non–AIDS-related pathologies. We investigated the correlation of cytokine responses with changes in CD4 T-cell levels and coinfection with hepatitis C virus (HCV) during highly active antiretroviral treatment (HAART).Methods.A total of 383 participants in the Women's Interagency HIV Study (212 with HIV monoinfection, 56 with HCV monoinfection, and 115 with HIV/HCV coinfection) were studied. HIV-infected women had <1000 HIV RNA copies/mL, 99.7% had >200 CD4 T cells/μL; 98% were receiving HAART at baseline. Changes in CD4 T-cell count between baseline and 2–4 years later were calculated. Peripheral blood mononuclear cells (PBMCs) obtained at baseline were used to measure interleukin 1β (IL-1β), interleukin 6 (IL-6), interleukin 10 (IL-10), interleukin 12 (IL-12), and tumor necrosis factor α (TNF-α) responses to Toll-like receptor (TLR) 3 and TLR4 stimulation.Results.Undetectable HIV RNA (<80 copies/mL) at baseline and secretion of IL-10 by PBMCs were positively associated with gains in CD4 T-cell counts at follow-up. Inflammatory cytokines (IL-1β, IL-6, IL-12, and TNF-α) were also produced in TLR-stimulated cultures, but only IL-10 was significantly associated with sustained increases in CD4 T-cell levels. This association was significant only in women with HIV monoinfection, indicating that HCV coinfection is an important factor limiting gains in CD4 T-cell counts, possibly by contributing to unbalanced persistent inflammation.Conclusions.Secreted IL-10 from PBMCs may balance the inflammatory environment of HIV, resulting in CD4 T-cell stability. [ABSTRACT FROM AUTHOR]

Objective: To evaluate the impact of hepatitis C virus (HCV) on the immune system before receipt of highly active antiretroviral therapy (HAART) and on immune recovery after receipt of HAART among human immunodeficiency virus (HIV)/HCV-coinfected women enrolled in the Women's Interagency HIV Study.Methods: The study included 294 HIV-infected women who initiated HAART and attended 2 follow-up visits. The women were grouped on the basis of positive HCV antibody and HCV RNA tests. There were 148 women who were HCV antibody negative, 34 who were HCV antibody positive but RNA negative, and 112 who were HCV antibody and RNA positive. Immune recovery was measured by flow-cytometric assessment for markers of activation and maturation on CD4+ and CD8+ T cells. Data analysis used repeated measures of variance.Results. HIV/HCV coinfection is associated with an increased number of CD4+ and CD8+ primed/memory T cells. HIV/HCV coinfection, however, did not affect any further decreases in CD4+ or CD4+ and CD8+ naive/memory T cell counts or enhanced T cell activation. HIV/HCV coinfection also did not affect HAART responses in the CD4+ and CD8+ T cell compartment.Conclusions: HCV does not affect immune responses to HAART in HIV/HCV-coinfected individuals but is associated with an expansion of CD4+ and CD8+ memory T cell subsets. Functional impairment in the CD4+ and CD8+ T cell compartments still needs to be assessed in coinfected patients. [ABSTRACT FROM AUTHOR]

Objective. To evaluate the impact of hepatitis C virus (HCV) on the immune system before receipt of highly active antiretroviral therapy (HAART) and on immune recovery after receipt of HAART among human immunodeficiency virus (HIV)/HCV-coinfected women enrolled in the Women's Interagency HIV Study. Methods. The study included 294 HIV-infected women who initiated HAART and attended 2 follow-up visits. The women were grouped on the basis of positive HCV antibody and HCV RNA tests. There were 148 women who were HCV antibody negative, 34 who were HCV antibody positive but RNA negative, and 112 who were HCV antibody and RNA positive. Immune recovery was measured by flow-cytometric assessment for markers of activation and maturation on CD4+ and CD8+ T cells. Data analysis used repeated measures of variance. Results. HIV/HCV coinfection is associated with an increased number of CD4+ and CD8+ primed/memory T cells. HIV/HCV coinfection, however, did not affect any further decreases in CD4+ or CD4+ and CD8+ naive/memory T cell counts or enhanced T cell activation. HIV/HCV coinfection also did not affect HAART responses in the CD4+ and CD8+ T cell compartment. Conclusions. HCV does not affect immune responses to HAART in HIV/HCV-coinfected individuals but is associated with an expansion of CD4+ and CD8+ memory T cell subsets. Functional impairment in the CD4+ and CD8+ T cell compartments still needs to be assessed in coinfected patients. [ABSTRACT FROM AUTHOR]

This study analyzed 4 cases of hepatitis C virus (HCV)-naive transfusion recipients who developed hepatitis after receiving blood from >1 HCV-infected donor. One recipient was exposed to 4 donors, 2 were exposed to 3 donors, and 1 was exposed to 2 donors. For 3 recipients, the strain from 1 of the donors predominated in all follow-up samples collected for 8-40 months. For 2 recipients, the strain from the second donor was occasionally detectable with sensitive strain-specific assays. For the fourth recipient, the initially dominant strain was later supplanted by a strain from the other donor. Simultaneous exposure to multiple HCV strains may result in concomitant infection by >1 strain, although a single strain rapidly establishes its dominance. These observations are compatible with the presence of competition among infecting HCV strains that results in the dominance of 1 strain and competitive exclusion or suppression of other strains. [ABSTRACT FROM AUTHOR]

Determines the phenotype of lymphoid cells harboring replicating hepatitis C virus (HCV) in human immunodeficiency virus type 1 positive subjects. Common etiologic agent of chronic hepatitis, cirrhosis and hepatocellular carcinoma; Presence of extrahepatic replication sites in HCV infection; Predicted secondary structures of consensus 5' untranslated region sequences.

The phenotypic characteristics of peripheral blood lymphocytes (PBLs) from responders and nonresponders to hepatitis B (HB) vaccine and their response to pokeweed mitogen (PWM) stimulation in vitro were compared. The nonresponders had significantly higher absolute numbers and percentages of T11+, HNK-1+, and T8+ lymphocytes. Also, after PWM stimulation, PBLs from HB-vaccine nonresponders had impaired IgG and IgM production and failed to produce antibodies to HB surface antigen in vitro. These findings suggest that healthy individuals who fail to produce such antibodies have a higher population of suppressor lymphocytes that alters their normal immune response to HB vaccination. [ABSTRACT FROM PUBLISHER]