ABSTRACT
Human immunodeficiency virus type 1 (HIV-1) has spread worldwide and has surpassed malaria as the leading cause of adult infectious disease mortality. Studies of large cohorts of HIV-1 infected individuals have shown that the clinical course and outcome of HIV-1 infection are highly variable among individuals. HIV-1 entry into target cells is mediated by binding of the viral envelope glycoprotein to CD4 on the target cell membrane, but CD4 expression is not sufficient for HIV-1 infection of target cells. Different HIV-1 isolates show distinct tropism for various CD4+ target cells, preferentially infecting either T cell lines or macrophages depending on usage of distinct chemokine receptors as coreceptors for infection. After becoming infected with HIV-1, individuals become acutely viremic and develop HIV-specific cytotoxic T lymphocytes (CTLs). CTLs control the viremia and infected individuals then enter a period of clinical latency that is highly variable in length.
