The Human T-Cell Lymphoma/Leukemia Viruses

Abstract

The primate T-cell lymphoma/leukemia viruses belong to an oncogenic genus of complex retroviruses. Members of this genus have been shown to be pathogenic in man. The human T-cell lymphoma/leukemia virus (HTLV) type I has been linked in the etiology of T-cell malignancies and “autoimmune-like” neurologic and rheumatic disorders; a related virus, HTLV-II, is becoming increasingly associated with similar disorders. Cell transformation is thought to be caused predominantly by the effects of the viral regulatory protein, Tax. An additional induced host cell molecule, adult T-cell lymphoma-derived factor, may contribute to cell immortalization. Like the DNA tumor viruses, HTLV activates transcription of cellular proto-oncogenes and inhibits cellular mechanisms of tumor suppression, cell cycle arrest, and apoptosis. However, individuals who are able to mount a strong cell-mediated immune response and limit viral entry into uninfected cells do not develop associated malignancies. Unfortunately, HTLV-induced malignancies are difficult to treat with conventional chemotherapy, and disease progression is often rapid with a median survival of less than 2 years. There are, however, some novel approaches that have yet to be fully tested that may have greater efficacy in the treatment of HTLV-induced diseases. In the future, better screening and detection methods, along with new vaccines and therapies, may contribute to the increased prevention and control of HTLV infection and its associated diseases.