Beld M, Penning M, Lukashov V, McMorrow M, Roos M, Pakker N, van den Hoek A, Goudsmit J
Department of Human Retrovirology, Academic Medical Centre, University of Amsterdam, The Netherlands.
Virology. 1998 May 10;244(2):504-12. doi: 10.1006/viro.1998.9130.
The 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/microliter (P = 0.001), but not in the population with CD4+ cell counts < 500 cells/microliter. 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.
这项回顾性队列研究的目的是评估1型人类免疫缺陷病毒（HIV）影响注射吸毒者丙型肝炎病毒（HCV）复制的机制。在1至9年的时间里，对19名HCV血清转化者的连续样本进行了病毒学（HCV和HIV RNA水平）和免疫学（CD4 +、CD8 +细胞计数以及抗CD3反应性）参数的测定。在这些受试者中，10名是HIV血清阴性（HIVneg），4名是HIV血清阳性（HIVpos），5名在观察期内发生了HIV血清转化（HIVsc）。HIVpos受试者的HCV RNA水平高于HIVneg受试者。在发生HIV血清转化的受试者中，HIV血清转化后HCV RNA水平立即显著升高（P < 0.0001），而在HIVpos和HIVneg受试者中，其随时间保持稳定。在HIVpos人群（R = -0.22，P < 0.05）和HIVneg人群（R = -0.45，P < 0.0001）中，HCV RNA均与CD4 +细胞计数呈负相关。此外，当根据CD4 +细胞计数对受试者进行分层时，发现CD4 +细胞计数> 500个/微升的HIVpos和HIVneg受试者之间的HCV RNA水平存在显著差异（P = 0.001），但在CD4 +细胞计数< 500个/微升的人群中未发现差异。在任何人群中，均未发现HCV RNA水平与CD8 +细胞计数或抗CD3反应性之间存在相关性。HIV感染和CD4 +细胞计数均显然与HCV RNA水平相关。HIV感染与HCV复制之间的直接关联（独立于CD4 +细胞计数）似乎比HIV诱导的CD4 +细胞减少与HCV复制之间的关联更强。我们得出以下结论：（i）HCV复制在某种程度上受到HIV存在的直接影响；（ii）HCV特异性宿主免疫部分控制HCV复制；（iii）当免疫系统因HIV受损时，HCV复制增加。
