Mankowski J L, Carter D L, Spelman J P, Nealen M L, Maughan K R, Kirstein L M, Didier P J, Adams R J, Murphey-Corb M, Zink M C
Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.
Am J Pathol. 1998 Oct;153(4):1123-30. doi: 10.1016/S0002-9440(10)65656-8.
Although many human immunodeficiency virus-infected individuals develop lymphocytic interstitial pneumonia, the roles of host and viral factors in the pathogenesis of pneumonia are not well defined. Human immunodeficiency virus-infected children with lymphocytic interstitial pneumonia have human immunodeficiency virus-specific cytotoxic T cells in pulmonary infiltrates, increased survival time, and a reduced incidence of opportunistic infections, suggesting that lymphocytic interstitial pneumonia may reflect an effective antiviral immune response. In this study, 20 macaques were inoculated with related macrophage-tropic simian immunodeficiency viruses and examined for pulmonary lesions and virus gene expression. Ten macaques developed moderate to severe pneumonia characterized by perivascular, peribronchial, and interstitial infiltrates of lymphocytes and macrophages. Large numbers of pulmonary cytotoxic lymphocytes were demonstrated in macaques with moderate to severe pneumonia (P < 0.05) by immunostaining for TIA-1. There was no difference in viral load between macaques with moderate to severe pneumonia and those with mild to no pulmonary lesions. In five macaques inoculated with the same virus swarm, there was a significant (P < 0.05) inverse correlation between the percentage decline in CD4+ T-cell counts and the severity of pulmonary lesions. Pulmonary infiltrates of cytotoxic lymphocytes, the lack of correlation between severity of pulmonary lesions and virus gene expression, and the inverse relationship between pneumonia and inmune status suggest that simian immunodeficiency virus pneumonia may represent an immunopathological response to macrophage-tropic virus.
尽管许多感染人类免疫缺陷病毒的个体都会发生淋巴细胞间质性肺炎，但宿主和病毒因素在肺炎发病机制中的作用尚未明确界定。患有淋巴细胞间质性肺炎的感染人类免疫缺陷病毒的儿童，其肺部浸润中有人类免疫缺陷病毒特异性细胞毒性T细胞，生存时间延长，机会性感染发生率降低，这表明淋巴细胞间质性肺炎可能反映了一种有效的抗病毒免疫反应。在本研究中，20只猕猴接种了相关的嗜巨噬细胞猿猴免疫缺陷病毒，并检查了肺部病变和病毒基因表达情况。10只猕猴发生了中度至重度肺炎，其特征为血管周围、支气管周围以及淋巴细胞和巨噬细胞的间质浸润。通过对TIA-1进行免疫染色，在患有中度至重度肺炎的猕猴中发现了大量肺部细胞毒性淋巴细胞（P < 0.05）。中度至重度肺炎的猕猴与轻度至无肺部病变的猕猴之间的病毒载量没有差异。在接种相同病毒株的5只猕猴中，CD4 + T细胞计数下降百分比与肺部病变严重程度之间存在显著的负相关（P < 0.05）。细胞毒性淋巴细胞的肺部浸润、肺部病变严重程度与病毒基因表达之间缺乏相关性，以及肺炎与免疫状态之间的负相关关系表明，猿猴免疫缺陷病毒肺炎可能代表了对嗜巨噬细胞病毒的一种免疫病理反应。
