U.S. Army Medical Research Institute of Infectious Diseases, Virology Division, Fort Detrick, MD 21702, USA.
J Virol. 2011 Oct;85(19):9929-44. doi: 10.1128/JVI.05356-11. Epub 2011 Jul 20.
Andes virus (ANDV) is associated with a lethal vascular leak syndrome in humans termed hantavirus pulmonary syndrome (HPS). In hamsters, ANDV causes a respiratory distress syndrome closely resembling human HPS. The mechanism for the massive vascular leakage associated with HPS is poorly understood; however, T cell immunopathology has been implicated on the basis of circumstantial and corollary evidence. Here, we show that following ANDV challenge, hamster T cell activation corresponds with the onset of disease. However, treatment with cyclophosphamide or specific T cell depletion does not impact the course of disease or alter the number of surviving animals, despite significant reductions in T cell number. These data demonstrate, for the first time, that T cells are not required for hantavirus pathogenesis in the hamster model of human HPS. Depletion of T cells from Syrian hamsters did not significantly influence early events in disease progression. Moreover, these data argue for a mechanism of hantavirus-induced vascular permeability that does not involve T cell immunopathology.
安第斯病毒（ANDV）与一种称为汉坦病毒肺综合征（HPS）的人类致命性血管渗漏综合征有关。在仓鼠中，ANDV 引起类似于人类 HPS 的呼吸窘迫综合征。与 HPS 相关的大量血管渗漏的机制尚未完全了解；然而，基于间接和推论证据，T 细胞免疫病理学已被牵连。在这里，我们表明，在 ANDV 挑战后，仓鼠 T 细胞的激活与疾病的发作相对应。然而，尽管 T 细胞数量显著减少，但环磷酰胺或特异性 T 细胞耗竭治疗并不影响疾病进程或改变存活动物的数量。这些数据首次表明，在人类 HPS 的仓鼠模型中，T 细胞不是汉坦病毒发病机制所必需的。从叙利亚仓鼠中耗尽 T 细胞并没有显著影响疾病进展的早期事件。此外，这些数据表明汉坦病毒诱导的血管通透性的机制不涉及 T 细胞免疫病理学。
