Abstract

The hematopoietic stem cell has long been hypothesized to be a target of human immunodeficiency virus type-1 (HIV) infection that limits the potential for compensatory immune cell production. Data have recently emerged documenting stem cell dysfunction in HIV disease and indicating that immune recovery from potent antiretroviral therapy is partly driven by new T-cell generation. Effects of HIV on stem cell physiology, however, appear to be indirect, as stem cells are highly resistant to HIV infection. Despite the presence of surface receptors for HIV, the hematopoietic stem cell is not infectible with HIV. However, stem transduction can be achieved with HIV constructs in which the envelope glycoproteins have been replaced by vesicular stomatitis virus G protein. Therefore, hematopoietic stem cells are likely participants in HIV-related cytopenias, but they are spared direct infection and can serve as a resource for cellular therapies for AIDS.