HIV-related interstitial lung disease.
The progressive breakdown of the cell-mediated immunity, which characterizes the natural history of HIV infection, invariably leads to the development of miscellaneous opportunistic infections or neoplasms involving a number of tissues, including the respiratory tract. In particular, given the extent and the severity of most infectious complications, it is not surprising that respiratory failure is a common finding in patients who have AIDS-related interstitial lung disease. Extensive knowledge of the sequence of events that starts with HIV infection of CD4+ cells and leads to the development of respiratory complications has been recently achieved. The present understanding of the pathogenesis of AIDS-related interstitial lung disease comes from the evaluation of cell populations retrieved from bronchoalveolar lavage fluid. In particular, the information gained from bronchoalveolar lavage studies led to the realization that HIV strains are present in the respiratory tract of HIV-seropositive subjects at all stages of infection. Furthermore, the characterization of bronchoalveolar lavage fluid cells proved to be central in evaluating the striking local immunologic reactions that can be detected in the lungs of these patients. Bronchoalveolar lavage studies have also demonstrated that local protective mechanisms may cause the shift toward accelerated progression to AIDS and the development of respiratory failure. This reviews briefly examines clinical aspects and cellular patterns of HIV infection in the respiratory tract. We will also consider data showing that HIV infection evokes an inflammatory response, initiated and sustained by cytotoxic T lymphocytes and macrophages and mediated by a number of cytokines that amplify host defenses as well as facilitate the spread of the retrovirus throughout the lower respiratory tract.
Semenzato
G
G
Padua University School of Medicine, Italy.
Agostini
C
C
D015658:HIV Infections / Q000150:complications* / Q000276:immunology; D006801:Humans; D017563:Lung Diseases, Interstitial / Q000209:etiology* / Q000276:immunology