Ikuta K
Section of Serology, Hokkaido University, Sapporo, Japan.
Hokkaido Igaku Zasshi. 1996 Jan;71(1):21-6.
HIV, the etiological agent of AIDS, induces depletion of CD4+T cells. Upon primary infection, there is an initial viremia that is followed rapidly by a cell-mediated immune response and apparent viral clearance. Thereafter, the persistence of low levels of HIV in the blood for years before the onset of the disease is facilitated by the ability of the virus to establish persistent and latent infection. Notwithstanding the latent form in most population, the clinical stage of disease is significantly associated with all measures of virus load levels. This may be mainly due to the function of HIV to induce apoptosis in a patients' uninfected CD4+T cells, as a bystander effect. Thus, the mechanisms that latently infect in the cells after HIV infection and stimulate active replication of HIV from the latency are essential for an understanding of the pathogenicity of the disease. Therefore, prophylactic and therapeutic trials should be focused to their effect to reduce the HIV load level.
艾滋病的病原体人类免疫缺陷病毒（HIV）会导致CD4+T细胞耗竭。初次感染时，会出现初始病毒血症，随后迅速出现细胞介导的免疫反应以及明显的病毒清除。此后，在疾病发作前的数年里，血液中持续存在低水平的HIV，这得益于该病毒建立持续潜伏感染的能力。尽管在大多数人群中处于潜伏形式，但疾病的临床阶段与病毒载量水平的所有指标均显著相关。这可能主要归因于HIV作为旁观者效应诱导患者未感染的CD4+T细胞凋亡的功能。因此，HIV感染后在细胞中潜伏感染并从潜伏期刺激HIV活跃复制的机制，对于理解该疾病的致病性至关重要。所以，预防和治疗试验应聚焦于它们降低HIV载量水平的效果。
