HIV probably enters the lung early during the course of infection and may constitute an important site for virus production in HIV infected individuals. It can be detected in the lung during the asymptomatic phase and the load increases as disease progresses. HIV is present in both alveolar macrophages and alveolar lymphocytes, as well as other cell types within the lung, and may have profound early effects on alveolar macrophage and T lymphocyte function resulting in a CD8 + alveolitis which, although initially may be protective, later appears to be suppressive towards HIVdirected cytolysis. The activation of alveolar macrophages by HIV and other infectious agents may, by release of proinflammatory cytokines such as TNFα and GM-CSF, lead to impaired gas exchange but also to firther HIV replication. Further refinement of our understanding of the interplay between the virus and the local response within the lung could allow the possibility of therapeutic immunomodulation with local and appropriate cytokine therapy to the lung to reduce the current morbidity and mortality from AIDS.