Innate immunity and chronic immune activation in HCV/HIV-1 co-infection

被引:46
作者
Gonzalez, Veronica D. [1 ]
Landay, Alan L. [2 ]
Sandberg, Johan K. [1 ]
机构
[1] Karolinska Univ Hosp Huddinge, Karolinska Inst, Dept Med, Ctr Infect Med, S-14186 Huddinge, Sweden
[2] Rush Univ, Med Ctr, Chicago, IL 60612 USA
基金
瑞典研究理事会;
关键词
HCV; HIV-1; Innate immunity; IFN alpha; Chronic immune activation; HEPATITIS-C-VIRUS; HUMAN-IMMUNODEFICIENCY-VIRUS; PLASMACYTOID DENDRITIC CELLS; NATURAL-KILLER-CELLS; CD1D-RESTRICTED NKT CELLS; HIV-INFECTED PATIENTS; DEPENDENT CELLULAR CYTOTOXICITY; ALPHA-2A PLUS RIBAVIRIN; CD4(+) T-LYMPHOCYTES; INTERFERON-ALPHA;
D O I
10.1016/j.clim.2009.12.005
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Innate immune responses are critical in the defense against viral infections. NK cells, myeloid and plasmacytoid dendritic cells, and invariant CD1d-restricted NKT cells mediate both effector and regulatory functions in this early immune response. In chronic uncontrolled viral infections such as HCV and HIV-1, these essential immune functions are compromised and can become a double edged sword contributing to the immunopathogenesis of viral disease. In particular, recent findings indicate that innate immune responses play a central role in the chronic immune activation which is a primary driver of HIV-1 disease progression. HCV/HIV-1 co-infection is affecting millions of people and is associated with faster viral disease progression. Here, we review the role of innate immunity and chronic immune activation in HCV and HIV-1 infection, and discuss how mechanisms of innate immunity may influence protection as well as immunopathogenesis in the HCV/HIV-1 co-infected human host. (C) 2009 Elsevier Inc. All rights reserved.
引用
收藏
页码:12 / 25
页数:14
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