Prevention of immunodeficiency virus induced CD4+ T-cell depletion by prior infection with a non-pathogenic virus.
Prevention of immunodeficiency virus induced CD4+ T-cell depletion by prior infection with a non-pathogenic virus.
复制标题
通过先前感染非致病性病毒来预防免疫缺陷病毒引起的 CD4 T 细胞耗竭。
DOI：
10.1016/j.virol.2008.03.037
复制
发表时间：
2008
期刊：
影响因子：
3.7
通讯作者：
VandeWoude,Sue
中科院分区：
文献类型：
--
作者：
Terwee,JulieA;Carlson,JenniferK;Sprague,WendyS;Sondgeroth,KerryS;Shropshire,SarahB;Troyer,JenniferL;VandeWoude,Sue
由CD4 + T细胞的严重损失引发的免疫失调是HIV诱导的发病机制的基础。用美洲狮中流行的非致病性慢病毒（美洲狮慢病毒，PLV或FIVpco）感染家猫，可预防随后的强毒FIV感染引起的外周血CD4 + T细胞耗竭。维持这一关键人群与FIV病毒血症的显著减少无关，支持直接病毒致细胞病变效应不是免疫缺陷主要原因的假设。虽然这种方法类似于用改良活疫苗免疫，但在受保护动物中未发现免疫相关性，如血清中和抗体或病毒特异性T细胞增殖反应。在保护组和未保护组之间观察到细胞因子转录谱的差异，最显著的是干扰素γ。这些数据为免疫应答的非适应性增强在预防CD4 + T细胞损失中的重要性提供了支持。
Immune dysregulation initiated by a profound loss of CD4+ T-cells is fundamental to HIV-induced pathogenesis. Infection of domestic cats with a non-pathogenic lentivirus prevalent in the puma (puma lentivirus, PLV or FIVpco) prevented peripheral blood CD4+ T-cell depletion caused by subsequent virulent FIV infection. Maintenance of this critical population was not associated with a significant decrease in FIV viremia, lending support to the hypothesis that direct viral cytopathic effect is not the primary cause of immunodeficiency. Although this approach was analogous to immunization with a modified live vaccine, correlates of immunity such as a serum-neutralizing antibody or virus-specific T-cell proliferative response were not found in protected animals. Differences in cytokine transcription profile, most notably in interferon gamma, were observed between the protected and unprotected groups. These data provide support for the importance of non-adaptive enhancement of the immune response in the prevention of CD4+ T-cell loss.