Temporal relationship between human immunodeficiency virus type 1 RNA levels in serum and cellular infectious load in periheral blood

Cross-sectional analysis of 252 paired serum and peripheral blood mononuclear cell (PBMC) samples derived from 54 human immunodeficiency virus type 1 (HIV-1)-infected persons revealed a correlation between HIV-1 RNA load in serum and infectious load in peripheral CD4 T cells after 18 months of follow-up and before an AIDS diagnosis (Pearson's correlation coefficient [r(p)] = .71, P <.001) and during antiviral treatment (r[p] = .78, P <.001). To gain insight into the temporal relationship between both measures of virus load, longitudinally obtained samples from 23 persons with various clinical courses (slow or rapid disease progression, long-term survival) and 22 persons undergoing antiviral therapy (zidovudine or didanosine, or both, or ritonavir) were analyzed. In general, the kinetics of changes in both measures of virus load were similar in the natural course of infection (78% of study participants) and during treatment (82% of participants). These findings suggest that PBMC and serum represent closely related, if not the same, viral compartment

Evidence that both HIV and HIV-induced immunodeficiency enhance HCV replication among HCV seroconverters

AbstractThe objective of this retrospective cohort study is to assess the mechanism by which human immunodeficiency virus type 1 (HIV) influences hepatitis C virus (HCV) replication in injecting drug users. Virological (HCV and HIV RNA levels) and immunological (CD4+, CD8+cell counts, and anti-CD3 reactivity) parameters were determined in 19 HCV seroconverters in sequential samples over a period of 1 to 9 years. Among these subjects, 10 were HIV-seronegative (HIVneg), 4 were HIV-seropositive (HIVpos), and 5 seroconverted for HIV (HIVsc) during the observation period. HCV RNA levels were higher in HIVpos subjects than in HIVneg subjects. In subjects seroconverting for HIV, HCV RNA levels increased significantly immediately after HIV seroconversion (P< 0.0001), while they remained stable over time in HIVpos and HIVneg subjects. HCV RNA correlated inversely with CD4+cell counts in both the HIVpos population (R= −0.22,P< 0.05) and the HIVneg population (R= −0.45,P< 0.0001). In addition, when subjects were stratified according to CD4+cell counts a significant difference was found in HCV RNA levels between HIVpos and HIVneg subjects with CD4+cell counts >500 cells/μl (P= 0.001), but not in the population with CD4+cell counts <500 cells/μl. In no population was a correlation found between HCV RNA levels and CD8+cell counts or anti-CD3 reactivity. Both HIV infection and CD4+cell counts are apparently associated with HCV RNA levels. The direct association, independent of CD4+cell counts, between HIV infection and HCV replication appears to be stronger than the association between HIV-induced CD4+cell decline and HCV replication. We conclude that (i) HCV replication is in some way directly influenced by the presence of HIV; (ii) HCV-specific host immunity controls, in part, HCV replication; and (iii) HCV replication increases when the immune system is impaired by HIV