Gummuluru S, Novembre F J, Seshi B, Dewhurst S
Department of Microbiology and Immunology, University of Rochester Medical Center, New York 14642, USA.
Virology. 1996 Jan 1;215(1):97-100. doi: 10.1006/viro.1996.0010.
The PBj14 isolate of simian immunodeficiency virus, SIVsmmPBj14, is an acutely pathogenic lentivirus that causes severe gastrointestinal disease in macaque monkeys. The studies reported here examine the basis for the enteropathic phenotype of SIVsmmPBj14, using flow cytometric analysis of cultured macaque lymphocytes and immunohistochemical staining of tissue specimens from virus-infected macaques. The data show that enteropathic molecular clones of SIVsmmPBj14 induce expression of the alpha E beta 7 integrin, which is believed to mediate mucosal retention of T-cells, whereas molecular clones from nonenteropathic derivatives of SIVsmmPBj14 do not do so. Thus, elevated expression of alpha E beta 7 may ber responsible, at least in part, for the accumulation of abnormally large numbers of T-cells within the intestinal mucosa during acute SIVsmmPBj14 infection.
猿猴免疫缺陷病毒的PBj14分离株，即SIVsmmPBj14，是一种急性致病性慢病毒，可在猕猴中引起严重的胃肠道疾病。本文报道的研究使用对培养的猕猴淋巴细胞进行流式细胞术分析以及对病毒感染猕猴的组织标本进行免疫组织化学染色，来探究SIVsmmPBj14肠道病变表型的基础。数据显示，SIVsmmPBj14的肠道病变分子克隆可诱导αEβ7整合素的表达，据信该整合素可介导T细胞在黏膜中的滞留，而来自SIVsmmPBj14非肠道病变衍生物的分子克隆则不会。因此，αEβ7的表达升高可能至少部分地导致了急性SIVsmmPBj14感染期间肠道黏膜内异常大量T细胞的积聚。
