生物谷報道：美英一項新的研究結(jié)果顯示，有關(guān)艾滋病病毒破壞人體免疫系統(tǒng)的傳統(tǒng)理論是錯誤的,。
據(jù)法新社報道,，此前科學(xué)家們一直認為,，艾滋病病毒可導(dǎo)致健康白細胞（可確認感染以使人體避免感染的Ｔ細胞）慢慢耗盡，它會在人的生命結(jié)束前讓被感染的Ｔ細胞復(fù)制大量微小病毒,。這種感染,、艾滋病
病毒復(fù)制、再感染和細胞壞死的持續(xù)性循環(huán)被稱為“失控”假說,。
但本期《公共醫(yī)學(xué)圖書館》（PLoS Medicine）雜志發(fā)表的研究報告顯示,，美英兩國研究人員通過一個簡易數(shù)學(xué)模型表明，“失控”模型應(yīng)在數(shù)月內(nèi)耗盡人體內(nèi)的健康Ｔ細胞,，但實際情況是健康Ｔ細胞需要數(shù)年時間才能耗盡,，是“一個漫長的過程”。研究人員因此認為,，艾滋病病毒在感染人體時需要一個漫長的適應(yīng)過程,。
據(jù)研究人員推斷，確定這一過程“將是對艾滋病特性的一種關(guān)鍵性認識,，并將指明新的潛在療法”,。
上述研究報告的主要撰稿人、亞特蘭大埃默里大學(xué)的安德魯·耶茨說：“艾滋病病毒會經(jīng)常進行變異……有多種途徑增強其適應(yīng)能力,，如加強感染新細胞的能力,、加大被感染細胞復(fù)制新病毒的數(shù)量以及加快被感染細胞復(fù)制新病毒的速度。”
他還說：“艾滋病病毒適應(yīng)假說還需要大量試驗調(diào)查加以證明,。這只是假說而已,。”
美國和英國的科學(xué)家近日研究發(fā)現(xiàn)，解釋艾滋病病毒（HIV）如何侵害人體免疫系統(tǒng)的一項受醫(yī)學(xué)家廣泛接受的理論可能不成立,。
這一研究結(jié)果發(fā)表在最新一期《公共科學(xué)圖書館·醫(yī)學(xué)》雜志上,。
法新社25日報道，科學(xué)家原先普遍認為,，HIV會感染人體體內(nèi)的T細胞,。這種健康的白細胞對外來病毒起識別作用，讓人體的免疫系統(tǒng)作出反應(yīng),，對抗病毒感染,。健康的T細胞在感染HIV后，會開始制造病毒細胞,，同時健康細胞數(shù)量降低,。這種病毒增多、健康細胞減少的理論被稱為“失控”說,。
但美英兩國科學(xué)家利用數(shù)學(xué)模型模擬“失控”說過程發(fā)現(xiàn),，根據(jù)“失控”說的理論模式，人體感染HIV后,，體內(nèi)的T細胞會在幾個月內(nèi)完全消失,，病人隨即死亡,。而實際上，艾滋病人從感染到死亡的過程長達數(shù)年,。
對于這一過程為何比理論上慢的原因,，科學(xué)家的解釋是，人體可能在T細胞減少過程中,，啟動了一種緩和過程,，減慢了T細胞的減少速度。
“病毒每時每刻都在發(fā)生變異,，根據(jù)達爾文的理論,，病毒可能在變異過程中進行了自我選擇，以適應(yīng)感染病毒的人體環(huán)境,。”研究小組負責人,、美國佐治亞州埃默里大學(xué)教授安德魯·耶茨說，“通過選擇性變異,，病毒可以更容易地感染新細胞,、使被感染細胞制造出新型病毒或者更快地制造病毒。”
研究人員認為,，這一發(fā)現(xiàn)可能為找到HIV的特性,、尋找新療法提供重要線索。耶茨說,，這種病毒適應(yīng)說目前尚處在假設(shè)階段,，有待更多試驗證明。（援引新華網(wǎng)）
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
原始出處：
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
全文鏈接：
http://medicine.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.pmed.0040177
