生物谷报道：美英一项新的研究结果显示，有关艾滋病病毒破坏人体免疫系统的传统理论是错误的。
据法新社报道，此前科学家们一直认为，艾滋病病毒可导致健康白细胞（可确认感染以使人体避免感染的Ｔ细胞）慢慢耗尽，它会在人的生命结束前让被感染的Ｔ细胞复制大量微小病毒。这种感染、艾滋病
病毒复制、再感染和细胞坏死的持续性循环被称为“失控”假说。
但本期《公共医学图书馆》（PLoS Medicine）杂志发表的研究报告显示，美英两国研究人员通过一个简易数学模型表明，“失控”模型应在数月内耗尽人体内的健康Ｔ细胞，但实际情况是健康Ｔ细胞需要数年时间才能耗尽，是“一个漫长的过程”。研究人员因此认为，艾滋病病毒在感染人体时需要一个漫长的适应过程。
据研究人员推断，确定这一过程“将是对艾滋病特性的一种关键性认识，并将指明新的潜在疗法”。
上述研究报告的主要撰稿人、亚特兰大埃默里大学的安德鲁·耶茨说：“艾滋病病毒会经常进行变异……有多种途径增强其适应能力，如加强感染新细胞的能力、加大被感染细胞复制新病毒的数量以及加快被感染细胞复制新病毒的速度。”
他还说：“艾滋病病毒适应假说还需要大量试验调查加以证明。这只是假说而已。”
美国和英国的科学家近日研究发现，解释艾滋病病毒（HIV）如何侵害人体免疫系统的一项受医学家广泛接受的理论可能不成立。
这一研究结果发表在最新一期《公共科学图书馆·医学》杂志上。
法新社25日报道，科学家原先普遍认为，HIV会感染人体体内的T细胞。这种健康的白细胞对外来病毒起识别作用，让人体的免疫系统作出反应，对抗病毒感染。健康的T细胞在感染HIV后，会开始制造病毒细胞，同时健康细胞数量降低。这种病毒增多、健康细胞减少的理论被称为“失控”说。
但美英两国科学家利用数学模型模拟“失控”说过程发现，根据“失控”说的理论模式，人体感染HIV后，体内的T细胞会在几个月内完全消失，病人随即死亡。而实际上，艾滋病人从感染到死亡的过程长达数年。
对于这一过程为何比理论上慢的原因，科学家的解释是，人体可能在T细胞减少过程中，启动了一种缓和过程，减慢了T细胞的减少速度。
“病毒每时每刻都在发生变异，根据达尔文的理论，病毒可能在变异过程中进行了自我选择，以适应感染病毒的人体环境。”研究小组负责人、美国佐治亚州埃默里大学教授安德鲁·耶茨说，“通过选择性变异，病毒可以更容易地感染新细胞、使被感染细胞制造出新型病毒或者更快地制造病毒。”
研究人员认为，这一发现可能为找到HIV的特性、寻找新疗法提供重要线索。耶茨说，这种病毒适应说目前尚处在假设阶段，有待更多试验证明。（援引新华网）
Figure 1.A Simple Model of Self-Renewing Memory CD4+ T Cell Homeostasis in the Absence of HIV Infection, with Density-Dependent Rates of Division and Death of Resting Cells
原始出处：
Understanding the Slow Depletion of Memory CD4+ T Cells in HIV Infection
Andrew Yates1,2*, Jaroslav Stark3,4, Nigel Klein5, Rustom Antia1, Robin Callard2,5
1 Department of Biology, Emory University, Atlanta, Georgia, United States of America, 2 Centre for Mathematics and Physics in the Life Sciences and Experimental Biology, University College London, London, United Kingdom, 3 Department of Mathematics, Imperial College, London, United Kingdom, 4 Centre for Integrative Systems Biology at Imperial College, Imperial College London, United Kingdom, 5 Immunobiology Unit, Institute of Child Health, London, United Kingdom
Background
The asymptomatic phase of HIV infection is characterised by a slow decline of peripheral blood CD4+ T cells. Why this decline is slow is not understood. One potential explanation is that the low average rate of homeostatic proliferation or immune activation dictates the pace of a “runaway” decline of memory CD4+ T cells, in which activation drives infection, higher viral loads, more recruitment of cells into an activated state, and further infection events. We explore this hypothesis using mathematical models.
Methods and Findings
Using simple mathematical models of the dynamics of T cell homeostasis and proliferation, we find that this mechanism fails to explain the time scale of CD4+ memory T cell loss. Instead it predicts the rapid attainment of a stable set point, so other mechanisms must be invoked to explain the slow decline in CD4+ cells.
Conclusions
A runaway cycle in which elevated CD4+ T cell activation and proliferation drive HIV production and vice versa cannot explain the pace of depletion during chronic HIV infection. We summarize some alternative mechanisms by which the CD4+ memory T cell homeostatic set point might slowly diminish. While none are mutually exclusive, the phenomenon of viral rebound, in which interruption of antiretroviral therapy causes a rapid return to pretreatment viral load and T cell counts, supports the model of virus adaptation as a major force driving depletion.
Funding: The authors received no specific funding for this study.
Competing Interests: The authors have declared that no competing interests exist.
Academic Editor: Rob J. De Boer, Utrecht University, The Netherlands
Citation: Yates A, Stark J, Klein N, Antia R, Callard R (2007) Understanding the Slow Depletion of Memory CD4+ T Cells in HIV Infection. PLoS Med 4(5): e177 doi:10.1371/journal.pmed.0040177
Received: August 7, 2006; Accepted: March 26, 2007; Published: May 22, 2007
全文链接：
http://medicine.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.pmed.0040177
