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Driving Forces of AIDS Pathogenesis:Massive CD4^+ T Lymphocyte Depletion and Abnormal Immune Activation

Driving Forces of AIDS Pathogenesis:Massive CD4^+ T Lymphocyte Depletion and Abnormal Immune Activation
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摘要 The occurrence of massive CD4+ T cell depletion is one of the most prominent characteristics of human immunodeficiency virus type 1 (HIV-1) infection during acute phase, resulting in unrestorable destruction to the immune system. The infected host undergoes an asymptomatic period lasting several years with low viral load and ostensibly healthy status, which is presumably due to virus-specific adaptive immune responses. In the absence of therapy, an overwhelming majority of cases develop to AIDS within 8-10 years of latent infection. In this review, we discuss the roles in AIDS pathogenesis played by massive CD4+ T lymphocytes depletion in gut-associated lymphoid tissue (GALT) during acute infection and abnormal immune activation emerging in the later part of chronic phase. The occurrence of massive CD4^+ T cell depletion is one of the most prominent characteristics of human immunodeficiency virus type 1 (HIV-1) infection during acute phase, resulting in unrestorable destruction to the immune system. The infected host undergoes an asymptomatic period lasting several years with low viral load and ostensibly healthy status, which is presumably due to virus-specific adaptive immune responses. In the absence of therapy, an overwhelming majority of cases develop to AIDS within 8-10 years of latent infection. In this review, we discuss the roles in AIDS pathogenesis played by massive CD4^+ T lymphocytes depletion in gut-associated lymphoid tissue (GALT) during acute infection and abnormal immune activation emerging in the later part of chronic phase.
出处 《Virologica Sinica》 SCIE CAS CSCD 2009年第6期501-508,共8页 中国病毒学(英文版)
基金 NSFC (30872357) CAS (KSCX2-YWR-144) MOST (2008zx10001-002, 2006CB504200)
关键词 人类免疫缺陷病毒 T淋巴细胞 四氯化碳 发病机制 艾滋病 活化 异常 驱动力 HIV/AIDS CD4^+ T cell depletion Gut-associated lymphoid tissue Immune activation Pathogenesis
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