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急性 SIV 感染在黑长尾猴中表现为淋巴结中病毒迅速清除,生发中心无有效感染。

Acute SIV infection in sooty mangabey monkeys is characterized by rapid virus clearance from lymph nodes and absence of productive infection in germinal centers.

机构信息

Division of Comparative Pathology, New England Primate Research Center, Harvard Medical School, Southborough, Massachusetts, USA.

出版信息

PLoS One. 2013;8(3):e57785. doi: 10.1371/journal.pone.0057785. Epub 2013 Mar 5.

Abstract

Lymphoid tissue immunopathology is a characteristic feature of chronic HIV/SIV infection in AIDS-susceptible species, but is absent in SIV-infected natural hosts. To investigate factors contributing to this difference, we compared germinal center development and SIV RNA distribution in peripheral lymph nodes during primary SIV infection of the natural host sooty mangabey and the non-natural host pig-tailed macaque. Although SIV-infected cells were detected in the lymph node of both species at two weeks post infection, they were confined to the lymph node paracortex in immune-competent mangabeys but were seen in both the paracortex and the germinal center of SIV-infected macaques. By six weeks post infection, SIV-infected cells were no longer detected in the lymph node of sooty mangabeys. The difference in localization and rate of disappearance of SIV-infected cells between the two species was associated with trapping of cell-free virus on follicular dendritic cells and higher numbers of germinal center CD4(+) T lymphocytes in macaques post SIV infection. Our data suggests that fundamental differences in the germinal center microenvironment prevent productive SIV infection within the lymph node germinal centers of natural hosts contributing to sustained immune competency.

摘要

淋巴组织免疫病理学是 AIDS 易感物种慢性 HIV/SIV 感染的一个特征性特征,但在 SIV 感染的自然宿主中不存在。为了研究导致这种差异的因素,我们比较了自然宿主黑长尾猴和非自然宿主猪尾猕猴在初次 SIV 感染期间生发中心的发展和外周淋巴结中的 SIV RNA 分布。尽管在感染后两周,两种物种的淋巴结中都检测到了感染 SIV 的细胞,但它们仅局限于免疫功能正常的猕猴淋巴结的副皮质区,而在 SIV 感染的猕猴的副皮质区和生发中心都可以看到。到感染后 6 周,黑长尾猴的淋巴结中不再检测到感染 SIV 的细胞。两种物种之间感染 SIV 的细胞的定位和消失速度的差异与滤泡树突状细胞上游离病毒的捕获以及 SIV 感染后猕猴生发中心 CD4(+) T 淋巴细胞数量的增加有关。我们的数据表明,生发中心微环境的根本差异阻止了 SIV 在自然宿主淋巴结生发中心的有效感染,从而导致持续的免疫能力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1ae/3589484/c25511dcae78/pone.0057785.g001.jpg

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