來自法國的一組科學家在4月9日表示,，他們期望能通過對一小部分未接受治療而能長時間對抗體內(nèi)HIV病毒的病人的研究來尋找到一種艾滋病疫苗,。
法國國家艾滋病研究機構的主任Jean-Francois Delfraissy表示：“有很小一部分的艾滋病人——大約少于艾滋病人總數(shù)的1%——能在其免疫系統(tǒng)內(nèi)部產(chǎn)生非常強大的抗病毒反應，這正是我們期望能從疫苗中獲得的效果,。”
Delfraissy和其他研究人員正在致力于研究這些HIV攜帶者是如何有效控制體內(nèi)的病毒的。他們的研究結(jié)果發(fā)表在美國刊物《美國國家科學院院刊》（PNAS）上,，文章說明了一些被稱為CD8的免疫細胞是如何幫助這一小部分病人阻止HIV感染的傳播過程的,。
這些病人雖然有很強的免疫力，但是他們?nèi)匀怀蔋IV陽性,，因為其體內(nèi)還是在源源不斷的產(chǎn)生對抗HIV的抗體,，但是他們并不需要進行治療。
因此科學家們表示,，CD8細胞在這一過程中起到的關鍵作用能幫助尋找到一種疫苗,，一種針對大部分免疫系統(tǒng)無法自發(fā)激活強大的抗HIV機制的病人的疫苗。
由于變異的非?？?，而且有很多對抗抗體的手段，HIV是疫苗研究人員遇到過的最可怕的敵人,。但是就在今年2月,，一個美國研究小組表示他們找到了在HIV病毒上存在一個關鍵的不變區(qū)域——這意味著他們找到了一個不變的攻擊目標。該小組還說在一些體內(nèi)長期存在病毒的人血液中找到了能識別這一區(qū)域的特殊抗體——b12,。
原始出處：http://www.physorg.com/news95359489.html
部分英文原文：
Published online before print April 11, 2007
Proc. Natl. Acad. Sci. USA, 10.1073/pnas.0611244104
Immunology
HIV controllers exhibit potent CD8 T cell capacity to suppress HIV infection ex vivo and peculiar cytotoxic T lymphocyte activation phenotype
( HIV suppression | CD8+ T cells | HLA-DR | CD38 )
Asier Sáez-Cirión , Christine Lacabaratz , Olivier Lambotte , Pierre Versmisse , Alejandra Urrutia , Faroudy Boufassa ¶, Françoise Barré-Sinoussi , Jean-François Delfraissy , Martine Sinet , Gianfranco Pancino ||, Alain Venet , and for the Agence Nationale de Recherches sur le Sida EP36 HIV Controllers Study Group
Unité de Régulation des Infections Rétrovirales, Institut Pasteur, 75725 Paris, France; Unité 802, Institut National de la Santé et de la Recherche Médicale, Faculté de Médecine Paris XI, 94276 Le Kremlin-Bicêtre, France; and Service de Médecine Interne et Maladies Infectieuses and ¶Unité 569, Institut National de la Santé et de la Recherche Médicale/Institut National des Etudes Démographiques, Hôpital Bicêtre, 94276 Le Kremlin-Bicêtre, France
Edited by Dan R. Littman, New York University Medical Center, New York, NY, and approved February 27, 2007 (received for review December 18, 2006)
Some rare HIV-1-infected individuals, referred to as HIV controllers (HIC), have persistently undetectable plasma viral load in the absence of therapy. This control of HIV-1 replication has been associated with a strong, multifunctional specific CD8+ T cell response. However, no direct link between this immune response and the control of viremia has so far been provided. We investigated parameters of specific CD8+ T cell response and in vitro susceptibility to HIV-1 infection in 11 HIC. We found high frequencies of HIV-specific CD8+ T cells. Interestingly, these cells expressed the activation marker HLA-DR but not CD38. This unique phenotype differentiates HIV-specific CD8+ T cells from HIC and noncontroller subjects and likely reflects a high potential to expand upon exposure to antigen and a capacity to exert effector functions. Accordingly, although CD4+ T cells from HIC were fully susceptible to HIV-1 superinfection, their CD8+ T cells effectively suppressed HIV-1 infection. Remarkably, this potent anti-HIV activity was observed without prior stimulation of CD8+ T cells. This activity was not mediated by secreted inhibitory factors but was due to the elimination of infected CD4+ T cells and was observed only with autologous CD4+ T cells, indicating an HLA-restricted cytotoxic mechanism. This constitutive antiviral capacity of CD8+ T cells could account for the control of viral replication in HIC.
