Activation-inactivation of HIV-1 in the lung.
The lung is prominently afflicted during the course of HIV-1 disease by both infectious and noninfectious complications. Direct or indirect effects of HIV-1 are likely central to the pathogenesis of these complications. Thus, any changes in viral load locally would negatively impact on the lung. This review focuses on the endogenous influences (immune effector cells, surfactant) and the exogenous factors (including infections such as tuberculosis and noninfectious exposures like cigarette smoke) that may contribute to activation or inactivation of HIV-1 in the lung.
Rich
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Department of Medicine, Case Western Reserve University, Cleveland, Ohio 44106-4984, USA. ear7@po.cwru.edu
D017088:AIDS-Related Opportunistic Infections / Q000503:physiopathology; D000163:Acquired Immunodeficiency Syndrome / Q000150:complications*; D015497:HIV-1 / Q000254:growth & development*; D006801:Humans; D008168:Lung / Q000503:physiopathology / Q000821:virology*; D016676:Macrophages, Alveolar / Q000502:physiology / Q000821:virology; D011663:Pulmonary Surfactants / Q000502:physiology; D012907:Smoking; D014397:Tuberculosis, Pulmonary / Q000209:etiology; D014775:Virus Activation
D011663:Pulmonary Surfactants