The Lentivirus genus, itself a subset of the Retroviridae family of RNA viruses, includes viruses that share a common replicative cycle, which is regulated by key events throughout the cycle. One such event in the viral life cycle is the expression of the viral genome regulated by the activity of the long terminal repeat (LTR). The LTR serves as a convergence point for transcription factors and elements of the transcriptional machinery from the host cell as well as virus-encoded proteins that enhance or modulate LTR activity and the subsequent expression of viral RNA and proteins. LTRs contain elements that interact with the basic transcriptional machinery of the host cell, transcription factors that are found in a wide range of cell types susceptible to infection, factors expressed in a cell-type specific pattern or a select subset of cells, and factors expressed in conjunction with cellular differentiation, activation, and progression through the cell cycle.

Infections by each of the lentiviruses, including the human immundeficiency virus types 1 and 2 (HIV-1 and HIV-2), simian immunodeficiency virus (SIV), feline immunodeficiency virus (FIV), visna virus, equine infectious anemia virus (EIAV), and caprine arthritis/encephalitis virus (CAEV), cause cellular and systemic events that initiate disease processes. While bovine immunodeficiency virus (BIV) infection does not appear to result in a clinical disease, it is nevertheless classified as a lentivirus based on its genomic organization and biological properties. Pathophysiologic events associated with each of these viruses (principally immunologic and neurologic deficiencies) require that the virus propagate efficiently in cell types able to support infection, including macrophages, which serve as hosts in all lentiviral infections. Productive progression through the viral replication cycle requires sufficient expression of viral regulatory and structural genes, which is in turn dependent on adequate function of the LTR within cells hosting the infection. LTR function has a direct impact on (i) the productive infection of the host cell,(ii) viral expression and assembly sufficient to drive viral loads to levels associated with pathogenesis and disease progression,(iii) the transition from a latency-like level of viral expression to a highly productive infection,(iv) production of cytotoxic viral proteins, and (v) production of sufficient virus for dissemination to compartments throughout the body, including the peripheral circulation, lymphatic system, brain, and lungs.