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Immune Response and Possible Causes of CD4+T-cell Depletion in HumanImmunodeficiency Virus (HIV) - 1 Infection

机译:人体免疫缺陷病毒(HIV)-1感染的免疫应答和CD4 + T细胞耗竭的可能原因

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In this review, immune response and possible causes of depletion of CD4+ T-cell counts in patients with humanimmunodeficiency (HIV)-1 infection, have been documented. HIV has been recognized as a global problem; however, thedeveloping countries are the most affected by epidemic diseases. Countries in the sub-Saharan Africa seem to bear thebulk of the HIV burden among the developing countries with about 24.7 million (≈ 63%) of all people living with HIVglobally in 2006. The major factor obstructing progress towards an effective vaccine to prevent or modulate HIV - 1 infectionis that the critical features needed for a protective immune response are not fully understood. Although, it has beenfound that potent neutralizing antibodies can protect against experimentally acquired HIV infection in animal models,they are scarcely generated in vivo in the infected person and neutralization resistant viral variants have been monitored todevelop rapidly in chronic infection. It is generally believed that cellular immune responses, particularly specific cytotoxicT lymphocytes (CTL), are significant in the host response to HIV - 1 infection. Scientists have observed that CTL developvery early in acute HIV - 1 infection, coincident with a rapid fall in plasma vireamia, whereas in chronic infection theirlevels are inversely related to viral load. However the potent HIV-specific CTL response ultimately fails to control HIVreplication. This could be as a consequence of the emergence of viral variants that escape CTL recognition or impairmentof CTL function.
机译:在这篇综述中,已记录了人类免疫缺陷病毒(HIV)-1感染患者的免疫应答和CD4 + T细胞计数耗尽的可能原因。艾滋病毒已被认为是全球性问题;然而,发展中国家受流行病的影响最大。撒哈拉以南非洲国家似乎承担了发展中国家的艾滋病毒负担的重担,2006年全球约有2470万艾滋病毒携带者(约占63%)。主要因素阻碍了预防或调节有效疫苗的进展HIV-1感染是保护性免疫反应所需的关键特征尚未完全了解。尽管已经发现有效的中和抗体可以在动物模型中预防实验获得的HIV感染,但是在感染者体内几乎不产生它们,并且已经监测到中和抗性病毒变体在慢性感染中迅速发展。通常认为,细胞免疫应答,特别是特异性细胞毒性T淋巴细胞(CTL),在宿主对HIV-1感染的应答中很重要。科学家观察到,在急性HIV-1感染中,CTL发育较早,与血浆病毒血症迅速下降相吻合,而在慢性感染中,其水平与病毒载量呈负相关。但是,有效的HIV特异性CTL反应最终无法控制HIV复制。这可能是由于出现了逃避CTL识别或CTL功能受损的病毒变体的结果。

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