Worldwide, chronic viral infections cause major health problems with severe morbidity and mortality. HIV and hepatitis C virus (HCV) manifest themselves as persistent infections, but they are entirely distinct viruses with distinct replication mechanisms, tropism, and kinetics. Coinfections with HCV among people with HIV are emerging as a growing problem. Cellular immune responses play an important role in viral clearance and disease pathogen-esis. However, cellular immunity to HIV and HCV is affected severely in chronic patients. Various hypotheses have been proposed to explain the dysfunctional T cell response, including viral escape mutations,exhaustion of the T cell compartment, and the activity of regulatory T cells. Also, modulation of the function ofdendritic cells (DC) has been suggested as one of the mechanisms used by persistent viruses to evade the immune system. In this review, we will focus on DC interactions with one murine persistent virus (lymphocytic choriomeningitis virus clone 13) and two human persistent viruses (HIV-1 and HCV),intending to examine if general strategies are used by persistent viruses to modulate the function of DC to improve our understanding of the mechanisms underlying the development and maintenance of viral persistence.

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Keywords HCV, HIV, Hepatitis, Hepatitis C virus, Human immunodeficiency virus 1, Human immunodeficiency virus infection, Immune evasion, LCMV, Lymphocytic choriomeningitis virus, alpha dystroglycan, alpha interferon, beta interferon, binding affinity, cell function, cell interaction, cell stimulation, cellular immunity, cytokine production, dendritic cell, hepatitis C, human, immune response, interleukin 12, macrophage, nonhuman, pathogenesis, persistent infection, priority journal, regulatory T lymphocyte, review, stromal cell derived factor 1, virus attachment, virus infection
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Journal Journal of Leukocyte Biology
Liu, B, Woltman, A.M, Janssen, H.L.A, & Boonstra, P.A. (2009). Modulation of dendritic cell function by persistent viruses. Journal of Leukocyte Biology (Vol. 85, pp. 205–214). doi:10.1189/jlb.0408241