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首页> 外文期刊>Current opinion in HIV and AIDS >HIV-1 replicative fitness in elite controllers.
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HIV-1 replicative fitness in elite controllers.

机译：精英控制者中的HIV-1复制适应性。

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PURPOSE OF REVIEW: Differential rates of disease progression are obviously multifactorial, but the virulence of the actual infecting virus is most frequently ignored as potential source of slow or rapid disease progression. In this review, the argument will be made that nearly all elite suppressors are infected by weak HIV-1 strain (in terms of replicative capacity). Whether this poor virus replication is the cause of elite suppression or the consequence of a strong immune response remains a leading question in the field. RECENT FINDINGS: Although numerous research studies have related HIV-1 replicative capacity/fitness in tissue culture to virulence within patients, this review will focus on several recent and key discoveries on the important role of HIV-1 fitness in elite suppression. First, elite suppressors appear to harbor HIV-1 variants that encode Gag, Pol, and Env proteins that are less efficient than their counterparts of HIV-1 in typical/chronic progressors. Second, the actual HIV-1 clone(s) that establish acute infection may be less fit in patients who become elite controllers as compared with typical progressors. Finally, the fitness costs of cytotoxic T lymphocyte escape in HIV-1 may be easily compensated by secondary mutations if the infecting strain is capable of high replication kinetics and rapid evolution. A strain with weak replicative capacity might not compensate for fitness loss or even generate the initial escape mutations. SUMMARY: A combination of good, anti-HIV-1 host genetics (e.g. HLA-B*57) along with infection by a 'whimpy' HIV-1 strain may be necessary for elite suppression, whereas only one of these may lead to slow progression and viremia.
机译：审查目的：疾病进展的差异率显然是多因素的，但是实际感染病毒的毒力最常被忽略，因为它是疾病缓慢或快速发展的潜在来源。在这篇综述中，将论证几乎所有的精英抑制因子都被弱的HIV-1株感染（就复制能力而言）。这种不良的病毒复制是造成精英抑制的原因还是强烈的免疫反应的结果，仍然是该领域的主要问题。最近的发现：尽管许多研究都将HIV-1复制在组织培养中的能力/适应性与患者体内的毒力相关，但本综述将侧重于关于HIV-1适应性在精英抑制中的重要作用的最新发现和关键发现。首先，精英抑制因子似乎带有编码Gag，Pol和Env蛋白的HIV-1变异体，这些变异体在典型/慢性进展者中效率不如HIV-1。其次，与典型的进展者相比，成为急性控制者的患者中，建立急性感染的实际HIV-1克隆可能不太适合。最后，如果感染菌株能够进行高复制动力学和快速进化，则可以通过二级突变轻松补偿HIV-1中细胞毒性T淋巴细胞逸出的适应性成本。复制能力较弱的菌株可能无法弥补适应性丧失，甚至无法产生初始逃逸突变。摘要：良好的抗HIV-1宿主遗传学（例如HLA-B * 57）与“狂躁” HIV-1菌株感染的结合可能是抑制精英的必要条件，而其中只有一种可能导致慢进展和病毒血症。

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