Stahl-Hennig C, Steinman R M, Tenner-Racz K, Pope M, Stolte N, Mätz-Rensing K, Grobschupff G, Raschdorff B, Hunsmann G, Racz P
German Primate Center, 37077 Göttingen, Germany.
Science. 1999 Aug 20;285(5431):1261-5. doi: 10.1126/science.285.5431.1261.
The early events during infection with an immunodeficiency virus were followed by application of pathogenic simian immunodeficiency virus atraumatically to the tonsils of macaques. Analyses by virologic assays and in situ hybridization revealed that the infection started locally in the tonsils, a mucosal-associated lymphoid organ, and quickly spread to other lymphoid tissues. At day 3, there were few infected cells, but then the number increased rapidly, reaching a high plateau between days 4 and 7. The infection was not detected in the dendritic cell-rich squamous epithelium to which the virus was applied; instead, it was primarily in CD4+ tonsillar T cells, close to the specialized antigen-transporting epithelium of the tonsillar crypts. Transport of the virus and immune-activating stimuli across this epithelium would allow mucosal lymphoid tissue to function in the atraumatic transmission of immunodeficiency viruses.
在用免疫缺陷病毒感染的早期事件之后,将致病性猿猴免疫缺陷病毒无创地应用于猕猴的扁桃体。通过病毒学检测和原位杂交分析发现,感染始于扁桃体(一种黏膜相关淋巴器官)局部,然后迅速扩散到其他淋巴组织。在第3天,感染细胞很少,但随后数量迅速增加,在第4天至第7天之间达到一个高平台期。在病毒所应用的富含树突状细胞的鳞状上皮中未检测到感染;相反,主要是在靠近扁桃体隐窝的特殊抗原转运上皮的CD4+扁桃体T细胞中。病毒和免疫激活刺激物穿过这种上皮的转运将使黏膜淋巴组织在免疫缺陷病毒的无创传播中发挥作用。