PATHOGENESIS OF SIMIAN IMMUNODEFICIENCY VIRUS PNEUMONIA - AN IMMUNOPATHOLOGICAL RESPONSE TO VIRUS

Although many human immunodeficiency virus-infected individuals develo p lymphocytic interstitial pneumonia, the roles of host and viral fact ors in the pathogenesis of pneumonia are not well defined. Human immun odeficiency virus-infected children with lymphocytic interstitial pneu monia have human immunodeficiency virus-specific cytotoxic T cells in pulmonary infiltrates, increased survival time, and a reduced incidenc e of opportunistic infections, suggesting that lymphocytic interstitia l pneumonia may reflect an effective antiviral immune response. In thi s study, 20 macaques mere inoculated with related macrophage-tropic si mian immunodeficiency viruses and examined for pulmonary lesions and v irus gene expression. Ten macaques developed moderate to severe pneumo nia characterized by perivascular, peribronchial, and interstitial inf iltrates of lymphocytes and macrophages. Large numbers of pulmonary cy totoxic lymphocytes were demonstrated in macaques with moderate to sev ere pneumonia (P < 0.05) by immunostaining for TIA-1. There was no dif ference in viral load between macaques with moderate to severe pneumon ia and those with mild to no pulmonary lesions. In five macaques inocu lated with the same virus swarm, there was a significant (P < 0.05) in verse correlation between the percentage decline in CD4+ T-cell counts and the severity of pulmonary lesions. Pulmonary infiltrates of cytot oxic lymphocytes, the lack of correlation between severity of pulmonar y lesions and virus gene expression, and the inverse relationship betw een pneumonia and immune status suggest that simian immunodeficiency v irus pneumonia may represent an immunopathological response to macroph age-tropic virus.