據參與研究工作的科學(xué)家介紹，這種新的治療方法既可以殺滅在人體內四處游蕩的病毒，還能夠殺滅隱藏在免疫細胞內的病毒。該項研究成果的價(jià)值在于它為全世界研究艾滋病治療的科學(xué)家指明了前進(jìn)的方向，為找到一種全新的具有創(chuàng )新性的艾滋病治療方法奠定了基礎。相關(guān)文章6月21日在線(xiàn)發(fā)表于《自然—醫學(xué)》。
迄今為止，抗艾滋病治療的療效一直不甚理想，原因是病毒隱藏在免疫系統細胞里，而目前使用的高效抗逆轉錄病毒療法對躲藏在免疫細胞內的病毒無(wú)計可施。加拿大和美國的研究人員成功地識別出那些躲藏有病毒的細胞，找到了病毒可以逃避現有治療的“隱身”機理。
參與研究工作的麥吉爾大學(xué)血液學(xué)家基恩·羅迪教授認為，該項研究成果首次證明所謂的艾滋病病毒潛伏池現象并不是因為抗逆轉藥物缺乏效力，而是由于病毒隱藏在兩種不同類(lèi)型的長(cháng)壽命CD4記憶免疫細胞內。艾滋病病毒潛伏池有幾種類(lèi)型，每一種類(lèi)型潛伏池都需要不同的治療方法來(lái)消除它們。一旦病毒隱藏在這些潛伏池細胞里，它們就會(huì )對其產(chǎn)生依賴(lài)。如果細胞存活，病毒就可以存活，但如果細胞死亡，則病毒也無(wú)法存活。因此，消滅這些免疫細胞就能夠殺滅這些隱藏其中的病毒?，F存的高效抗逆轉錄病毒療法可以殺滅在體內流傳的病毒，但是無(wú)法對付隱藏在免疫系統細胞內的病毒。
主持研究工作的蒙特利爾大學(xué)塞卡里教授表示，該研究結果與用于治療白血病采取的策略相似，即同樣是定向化療，并同時(shí)與定向免疫治療相結合。這種方法既可以殺滅細胞中的病毒，同時(shí)也為免疫系統留出時(shí)間再生健康細胞。
研究人員認為，目前所得到的成果為開(kāi)發(fā)出全新的抗艾滋病毒治療方法提供了一個(gè)重要的選項，但要進(jìn)入實(shí)際應用還需要若干年進(jìn)一步的研究工作。（生物谷Bioon.com）
生物谷推薦原始出處：
Nature Medicine 21 June 2009 | doi:10.1038/nm.1972
HIV reservoir size and persistence are driven by T cell survival and homeostatic proliferation
Nicolas Chomont1,2,3, Mohamed El-Far1,2,3, Petronela Ancuta3, Lydie Trautmann1,2,3, Francesco A Procopio1,2,3, Bader Yassine-Diab1,2,3, Geneviève Boucher1, Mohamed-Rachid Boulassel4, Georges Ghattas5, Jason M Brenchley6, Timothy W Schacker7, Brenna J Hill8, Daniel C Douek8, Jean-Pierre Routy4,9, Elias K Haddad1,2,3,9 & Rafick-Pierre Sékaly1,2,3,9,10,11
Abstract
HIV persists in a reservoir of latently infected CD4+ T cells in individuals treated with highly active antiretroviral therapy (HAART). Here we identify central memory (TCM) and transitional memory (TTM) CD4+ T cells as the major cellular reservoirs for HIV and find that viral persistence is ensured by two different mechanisms. HIV primarily persists in TCM cells in subjects showing reconstitution of the CD4+ compartment upon HAART. This reservoir is maintained through T cell survival and low-level antigen-driven proliferation and is slowly depleted with time. In contrast, proviral DNA is preferentially detected in TTM cells from aviremic individuals with low CD4+ counts and higher amounts of interleukin-7–mediated homeostatic proliferation, a mechanism that ensures the persistence of these cells. Our results suggest that viral eradication might be achieved through the combined use of strategic interventions targeting viral replication and, as in cancer, drugs that interfere with the self renewal and persistence of proliferating memory T cells.
1 Laboratoire d'Immunologie, Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CR-CHUM) Saint-Luc, Montréal, Québec, Canada.
2 Laboratoire d'Immunologie, Département de Microbiologie et d'Immunologie, Université de Montréal, Québec, Canada.
3 Institute National de la Santé et de la Recherche Médicale U743, CR-CHUM, Université de Montréal, Montréal, Québec, Canada.
4 Immunodeficiency Service and Division of Hematology, Royal Victoria Hospital, McGill University Health Centre (MUHC), McGill University, Montréal, Québec, Canada.
5 Department of Gastroenterology, MUHC, Montréal, Québec, Canada.
6 Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, US National Institutes of Health, Bethesda, Maryland, USA.
7 Department of Medicine, University of Minnesota, Minneapolis, Minnesota, USA.
8 Human Immunology Section, Vaccine Research Center, National Institute of Allergy and Infectious Diseases, US National Institutes of Health, Bethesda, Maryland, USA.
9 Department of Microbiology and Immunology, McGill University, Montréal, Québec, Canada.
10 Department of Microbiology and Immunology, Oregon Health and Science University, Portland, Oregon, USA.
11 Vaccine and Gene Therapy Institute, Port-Ste Lucy, Florida, USA.
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