Laskus Tomasz, Kibler Karen V, Chmielewski Marcin, Wilkinson Jeffrey, Adair Debra, Horban Andrzej, Stańczak Grzegorz, Radkowski Marek
Department of Immunopathology, Warsaw Medical University, Warsaw, Poland.
PLoS One. 2013 Oct 1;8(10):e75921. doi: 10.1371/journal.pone.0075921. eCollection 2013.
Hepatitis C virus (HCV) coinfection was reported to negatively affect HIV disease and HIV infection has a deleterious effect on HCV-related liver disease. However, despite common occurrence of HCV/HIV coinfection little is known about the mechanisms of interactions between the two viruses.
We studied CD4+ and CD8+ T cell and CD19+ B cell apoptosis in 104 HIV-positive patients (56 were also HCV-positive) and in 22 HCV/HIV-coinfected patients treated for chronic hepatitis C with pegylated interferon and ribavirin. We also analyzed HCV/HIV coinfection in a Daudi B-cell line expressing CD4 and susceptible to both HCV and HIV infection. Apoptosis was measured by AnnexinV staining.
HCV/HIV coinfected patients had lower CD4+ and CD8+ T cell apoptosis and higher CD19+ B cell apoptosis than those with HIV monoinfection. Furthermore, anti-HCV treatment of HCV/HIV coinfected patients was followed by an increase of CD4+ and CD8+ T cell apoptosis and a decrease of CD19+ B cell apoptosis. In the Daudi CD4+ cell line, presence of HCV infection facilitated HIV replication, however, decreased the rate of HIV-related cell death.
In HCV/HIV coinfected patients T-cells were found to be destroyed at a slower rate than in HIV monoinfected patients. These results suggest that HCV is a molecular-level determinant in HIV disease.
据报道,丙型肝炎病毒(HCV)合并感染对HIV疾病有负面影响,而HIV感染对HCV相关肝病也有有害影响。然而,尽管HCV/HIV合并感染很常见,但对于这两种病毒之间相互作用的机制却知之甚少。
我们研究了104例HIV阳性患者(其中56例也为HCV阳性)以及22例接受聚乙二醇干扰素和利巴韦林治疗慢性丙型肝炎的HCV/HIV合并感染患者的CD4 +和CD8 + T细胞以及CD19 + B细胞凋亡情况。我们还分析了在表达CD4且对HCV和HIV感染均敏感的Daudi B细胞系中的HCV/HIV合并感染情况。通过膜联蛋白V染色测量细胞凋亡。
与单纯HIV感染患者相比,HCV/HIV合并感染患者的CD4 +和CD8 + T细胞凋亡较低,而CD19 + B细胞凋亡较高。此外,对HCV/HIV合并感染患者进行抗HCV治疗后,CD4 +和CD8 + T细胞凋亡增加,而CD19 + B细胞凋亡减少。在Daudi CD4 +细胞系中,HCV感染的存在促进了HIV复制,然而,降低了HIV相关细胞死亡的速率。
在HCV/HIV合并感染患者中,发现T细胞被破坏的速度比单纯HIV感染患者慢。这些结果表明,HCV是HIV疾病中的分子水平决定因素。