Important note: Information in this article was accurate in 1992. The state of the art may have changed since the publication date.
MOLECULAR BIOLOGY OF HUMAN RETROVIRUSES AND THEIR RELATION TO CANCER
Molecular Foundations of Oncology. Broder S, ed. Baltimore, MD, Williams and Wilkins, p. 229-63, 1991.. Unique Identifier : AIDSLINE ICDB/92680281 Daefler S; Wong-Staal F; Dept. of Medicine, New York Univ. Medical Center, New York, NY
Abstract:
Since the beginning of the 20th century, retroviruses have been recognized as the cause of a variety of diseases in several animal species. Recently, there has been an explosion of knowledge concerning human retrovirology. Molecular aspects of human retroviruses are reviewed, including historical perspective; classification; pathology of retroviral infection in humans; retroviral genomic structure (human T lymphotropic virus [HTLV]-I, HTLV-II, HIV-1, HIV-2, and human foamy viruses); retroviral life cycle; expression of viral proteins; mechanism of cell transformation; HTLV-I- and HTLV-II-associated leukemogenesis; and tumor development in HIV-1 and HIV-2 infection. The known pathogenic human retroviruses fall into two major groups, the HTLVs causing predominantly leukemia and the HIVs causing predominantly immunodeficiency. Although these viruses follow different evolutionary lineages and belong to different retrovirus subgroups, they have remarkably similar biological and molecular properties. Both virus groups infect CD4+ helper T lymphocytes as a major target cell and both affect the immune system. Both induce disorders involving the CNS through unknown, although probably distinct, mechanisms. Both are associated with development of secondary malignancies, a probable common pathway being chronic antigenic stimulation of B cells, leading to the development of B-cell lymphomas. However, the most remarkable parallels lie in their complex strategies of virus regulation, which are fundamental to the establishment of clinical latency, and in the mechanisms of action of the viral regulatory proteins. The Tax and Tat proteins increase the level of transcribed viral mRNA and also affect cellular functions because they can transactivate heterologous genes. The role of Tat as a growth factor for Kaposi's sarcoma-derived cells provides a defined link between HIV infection and KS development. The Rex and Rev proteins are novel transactivators that regulate processing of viral precursor mRNA via a common mechanism. Other HIV-accessory genes such as vif, nef, vpr, vpu, and vpx also may play some role, mostly undefined as yet, in virus replication. (220 Refs)
Keywords: Acquired Immunodeficiency Syndrome/PHYSIOPATHOLOGY Base Sequence Genome, Viral Human HIV Infections/PHYSIOPATHOLOGY HTLV-I Infections/PHYSIOPATHOLOGY HTLV-II Infections/PHYSIOPATHOLOGY Molecular Sequence Data Neoplasms/*GENETICS/*MICROBIOLOGY Retroviridae/*GENETICS/PHYSIOLOGY Retroviridae Infections/GENETICS/*PHYSIOPATHOLOGY RNA, Viral/GENETICS Viral Proteins/GENETICS MONOGRAPH REVIEW, ACADEMIC REVIEW 920630
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Important note: Information in this article was accurate in 1992. The state of the art may have changed since the publication date.
