Pathogenesis of simian immunodeficiency virus pneumonia: An immunopathological response to virus

Joseph L Mankowski, Darryl L. Carter, Jeffrey P. Spelman, Michele L. Nealen, Kevin R. Maughan, Lynn M. Kirstein, Peter J. Didier, Robert John Adams, Michael Murphey-Corb, Mary Christine Zink

Research output: Contribution to journalArticle

Abstract

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 immune status suggest that simian immunodeficiency virus pneumonia may represent an immunopathological response to macrophage-tropic virus.

Original languageEnglish (US)
Pages (from-to)1123-1130
Number of pages8
JournalAmerican Journal of Pathology
Volume153
Issue number4
StatePublished - Oct 1998

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Simian Immunodeficiency Virus
Pneumonia
Macaca
Viruses
Lung
Interstitial Lung Diseases
Macrophages
HIV
Lymphocytes
T-Lymphocytes
Gene Expression
Opportunistic Infections
CD4 Lymphocyte Count
Viral Load
Antiviral Agents
Incidence

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

Cite this

Mankowski, J. L., Carter, D. L., Spelman, J. P., Nealen, M. L., Maughan, K. R., Kirstein, L. M., ... Zink, M. C. (1998). Pathogenesis of simian immunodeficiency virus pneumonia: An immunopathological response to virus. American Journal of Pathology, 153(4), 1123-1130.

Pathogenesis of simian immunodeficiency virus pneumonia : An immunopathological response to virus. / Mankowski, Joseph L; Carter, Darryl L.; Spelman, Jeffrey P.; Nealen, Michele L.; Maughan, Kevin R.; Kirstein, Lynn M.; Didier, Peter J.; Adams, Robert John; Murphey-Corb, Michael; Zink, Mary Christine.

In: American Journal of Pathology, Vol. 153, No. 4, 10.1998, p. 1123-1130.

Research output: Contribution to journalArticle

Mankowski, JL, Carter, DL, Spelman, JP, Nealen, ML, Maughan, KR, Kirstein, LM, Didier, PJ, Adams, RJ, Murphey-Corb, M & Zink, MC 1998, 'Pathogenesis of simian immunodeficiency virus pneumonia: An immunopathological response to virus', American Journal of Pathology, vol. 153, no. 4, pp. 1123-1130.
Mankowski JL, Carter DL, Spelman JP, Nealen ML, Maughan KR, Kirstein LM et al. Pathogenesis of simian immunodeficiency virus pneumonia: An immunopathological response to virus. American Journal of Pathology. 1998 Oct;153(4):1123-1130.
Mankowski, Joseph L ; Carter, Darryl L. ; Spelman, Jeffrey P. ; Nealen, Michele L. ; Maughan, Kevin R. ; Kirstein, Lynn M. ; Didier, Peter J. ; Adams, Robert John ; Murphey-Corb, Michael ; Zink, Mary Christine. / Pathogenesis of simian immunodeficiency virus pneumonia : An immunopathological response to virus. In: American Journal of Pathology. 1998 ; Vol. 153, No. 4. pp. 1123-1130.
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