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Glances in Immunology of HIV and HCV Infection

DOI: 10.1155/2012/434036

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Since the identification of HIV and HCV much progress has been made in the understanding of their life cycle and interaction with the host immune system. Despite these viruses markedly differ in their virological properties and in their pathogenesis, they share many common features in their immune escape and survival strategy. Both viruses have developed sophisticated ways to subvert and antagonize host innate and adaptive immune responses. In the last years, much effort has been done in the study of the AIDS pathogenesis and in the development of efficient treatment strategies, and a fatal infection has been transformed in a potentially chronic pathology. Much of this knowledge is now being transferred in the HCV research field, especially in the development of new drugs, although a big difference still remains between the outcome of the two infections, being HCV eradicable after treatment, whereas HIV eradication remains at present unachievable due to the establishment of reservoirs. In this review, we present current knowledge on innate and adaptive immune recognition and activation during HIV and HCV mono-infections and evasion strategies. We also discuss the genetic associations between components of the immune system, the course of infection, and the outcome of the therapies. 1. Introduction 1.1. Human Immunodeficiency Virus Infection Human immunodeficiency virus (HIV) is a retrovirus of the Lentiviridae family. This positive strand RNA virus infects specific cell populations of the immune system through its receptor specificity. At present, more than 33 million people are infected with HIV. HIV infection is characterized by an acute and a chronic phase, possibly leading to AIDS. Immediately after infection the viral load increases with exponential growth kinetics and CD4+ T cells rapidly decline [1, 2]. The peak of this growth curve coincides with the onset of a strong host immune response resulting in decreasing viral load and increasing number of circulating virus-specific CD4+ T cells. Then, the acute phase of HIV infection is accompanied by a selective and dramatic depletion of CD4+CCR5+ memory T cells predominantly from mucosal surfaces. This loss is largely irreversible and ultimately leads to the failure of the host immune defenses to clear the infection [3, 4]. This allows HIV to establish life-long latency and chronic infection. Over the chronic phase of infection, the viral load remains stable, whereas CD4+ T cell levels gradually decline [5]. The chronic phase is clinically latent, but eventually without therapeutic intervention, the

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