Guo Ming, Xian Qiao-Yang, Rao Yan, Zhang Jing, Wang Yong, Huang Zhi-Xiang, Wang Xin, Bao Rong, Zhou Li, Liu Jin-Biao, Tang Zhi-Jiao, Guo De-Yin, Qin Chuan, Li Jie-Liang, Ho Wen-Zhe
School of Basic Medical Sciences, Center for Animal Experiment/Animal Biosafety Level III Laboratory, Wuhan University Wuhan, Hubei, China.
Key Laboratory of Human Diseases Comparative Medicine, Ministry of Health, Institute of Laboratory Animal Science, Chinese Academy of Medical Sciences and Comparative Medicine Center, Peking Union Medical College Beijing, China.
Front Microbiol. 2017 Jan 13;7:2174. doi: 10.3389/fmicb.2016.02174. eCollection 2016.
Tuberculosis (TB) is a common opportunistic infection and the leading cause of death for human immunodeficiency virus (HIV)-infected patients. Thus, it is necessary to understand the pathogenetic interactions between and HIV infection. In this study, we examined and/or simian immunodeficiency virus (SIV) infection of Chinese rhesus macaques. While there was little evidence that enhanced SIV infection of macaques, SIV could facilitate infection as demonstrated by X-rays, pathological and microbiological findings. Chest X-rays showed that co-infected animals had disseminated lesions in both left and right lungs, while mono-infected animals displayed the lesions only in right lungs. Necropsy of co-infected animals revealed a disseminated infection not only in the lungs but also in the extrapulmonary organs including spleen, pancreas, liver, kidney, and heart. The bacterial counts in the lungs, the bronchial lymph nodes, and the extrapulmonary organs of co-infected animals were significantly higher than those of mono-infected animals. The mechanistic studies demonstrated that two of three co-infected animals had lower levels of specific IFN-γ and IL-22 in PBMCs than mono-infected animals. These findings suggest that Chinese rhesus macaque is a suitable and alternative non-human primate model for SIV/ coinfection studies. The impairment of the specific anti-TB immunity is likely to be a contributor of SIV-mediated enhancement infection.
结核病（TB）是一种常见的机会性感染，也是人类免疫缺陷病毒（HIV）感染患者的主要死因。因此，有必要了解结核菌与HIV感染之间的致病相互作用。在本研究中，我们检测了中国恒河猴的结核菌和/或猴免疫缺陷病毒（SIV）感染情况。虽然几乎没有证据表明结核菌会增强猕猴的SIV感染，但如X线、病理和微生物学检查结果所示，SIV可促进结核菌感染。胸部X线显示，合并感染的动物左右肺均有播散性病变，而单纯结核菌感染的动物仅右肺有病变。对合并感染动物的尸检显示，结核菌不仅在肺部播散感染，还在包括脾脏、胰腺、肝脏、肾脏和心脏在内的肺外器官播散感染。合并感染动物肺部、支气管淋巴结和肺外器官中的细菌计数显著高于单纯结核菌感染的动物。机制研究表明，三只合并感染动物中有两只外周血单个核细胞（PBMC）中结核菌特异性干扰素-γ和白细胞介素-22水平低于单纯结核菌感染的动物。这些发现表明，中国恒河猴是SIV/结核菌合并感染研究的合适且可替代的非人灵长类动物模型。特异性抗结核免疫受损可能是SIV介导的结核菌感染增强的一个因素。
