The human CD4+ T lymphocytes in the peripheral blood represent a major target for HIV-1 infection in vivo. In the quiescent state T lymphocytes are nonpermissive for the propagation of HIV-1. Antigenic or mitogenic stimulation of T lymphocytes triggers a cascade of biochemical events that lead to cellular proliferation and activation of transcription and replication of HIV-1. Transcription of HIV-1 provirus in infected T cells is regulated by the interaction of both viral proteins and cellular transcription factors with the viral long terminal repeat (LTR) sequences. HIV-1 LTR has been shown to contain recognition sequences for many cellular transcription factors. These include both positive and negative regulatory factors. Interplay of cellular proteins involve both the upstream and downstream regions of the viral LTR. Our full understanding of the transcriptional regulation of HIV-1 provirus will require isolation and characterization of each of these cellular factors which bind to the HIV-1 LTR. Mutational analyses of HIV-1 LTR indicate that not all these various cellular factors are absolutely essential for the regulation of LTR-mediated viral gene expression, but their presence or absence may determine the course of HIV-1 replication in the infected cells. A balance between the inhibitory host transcription factors and the stimulatory cellular and/or viral protein factors possibly determine the final consequence of HIV-1 replication and pathogenesis.