HIV replication and pulmonary opportunistic infections.

The lung is a priviledged target of opportunistic pathogens during HIV infection, dike to the dramatic immunodeficiency which characterizes the disease. Proviral forms of the virus are frequently detected in the lung, particularly in macrophages, which consitute an important viral reservoir and in T lymphocytes. The frequency of these proviral forms increases in the lung with the progression of the HIV disease. Some opportunistic pathogens themselves, or the mediators produced during immune responses toward these pathogens, are able to activate in vitro the HIV replication. An important increase of viral load is observed in the lung during P. carinii pneumonia and during tuberculosis. It has been shown that tuberculosis generated a micro-environment able to activate T lymphocytes present at the site of the disease and to increase their productive infection by HIV. TNF alpha and IL6, among other cytokines, could be involved in this phenomenon. The massive replication of HN during pulmonary infections could influence the general prognosis of the disease through the increase of the systemic vii al lend. In this context, new therapeutic strategies might have to be defined, including not only a wider prophylaxis but also antiretroviral treatments at the rime of infectious episodes.