The lung is prominently afflicted during the course of HIV-1 disease b
y both infectious and noninfectious complications. Direct or indirect
effects of HIV-1 are likely central to the pathogenesis of these compl
ications. Thus, any changes in viral load locally would negatively imp
act on the lung. This review focuses on the endogenous influences (imm
une effector cells, surfactant) and the exogenous factors (including i
nfections such as tuberculosis and noninfectious exposures like cigare
tte smoke) that may contribute to activation or inactivation of HIV-1
in the lung.