HCV–HIV Coinfection Simple Messages from a Complex Disease 英文参考文献.docVIP

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HCV–HIV Coinfection Simple Messages from a Complex Disease 英文参考文献.doc

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HCV–HIV Coinfection Simple Messages from a Complex Disease 英文参考文献

Research In Translation HCV–HIV Coinfection: Simple Messages from a Complex Disease Paul Klenerman , Arthur Kim * H epatitis C virus (HCV) and HIV infection are both major global health problems, each with their own speci?c unsolved and dif?cult issues of prevention, pathogenesis, and therapy. For HIV, many of the clinical problems experienced are related to loss of immunological control over relatively commonly encountered pathogens. In most of these cases (e.g., cytomegalovirus [CMV], Pneumocystis jiroveci, human herpesvirus-8), normal immunological control is quite ef?cient, and these organisms behave as “opportunists.” HCV is slightly different, in that immunological control in normal HIV-uninfected individuals is often poor, and HCV infection alone can lead to the gradual evolution of end- stage liver disease in normal hosts. However, although a consensus is forming about the basic details of the immune responses associated with acute control of HCV monoinfection, the long-term relationships between immune responses, viral load, and most importantly, disease progression in those who are persistently infected are still poorly understood. HIV–HCV coinfection is a problem of substantial size. Overall the ?gures for coinfection rates are very striking— around one in 10 of those infected with HIV globally are also HCV infected (around 4–5 million) [1]. In the West, however, the infection rate is one in four, and in speci?c risk groups, such as intravenous drug users, the ?gure rises to up to 50%–95%, regardless of global location. This re?ects the fact that HCV is relatively easy to spread through percutaneous infection, while relatively harder to spread through sexual contact. doi:10.1371/journal.pmed.0040240.g001 Figure 1. Immunologic Control of HCV Pathogenesis In a normal HCV monoinfection, HCV-speci?c CD4 and CD8 T cells are mobilized to contain infection. If infection is not cleared, such T cells contribute to antiviral effects, proin?ammatory effects, and