MOLECULAR ANALYSES OF THE BIOLOGY AND PATHOGENESIS OF THE HUMAN T-LYMPHOTROPIC RETROVIRUSES

Important note: Information in this article was accurate in 1988. The state of the art may have changed since the publication date.

MOLECULAR ANALYSES OF THE BIOLOGY AND PATHOGENESIS OF THE HUMAN T-LYMPHOTROPIC RETROVIRUSES

Diss Abstr Int (Sci); 48(2):348 1987. Unique Identifier : AIDSLINE ICDB/88639110
Feinberg MB; Stanford University

Abstract: The studies contained in this dissertation were undertaken to elucidate salient aspects of the biology and pathogenic processes of the human T-lymphotropic retroviruses. Studies directed at the mechanism of lymphocyte transformation by human T-lymphotropic virus type I (HTLV-I) (the etiologic agent of adult T-cell leukemia) resulted in the definition of structure and activities of a viral gene known as tat-l. The tat-l gene appears to act to increase transcription from genetic regulatory elements contained within the HTLV-I virus, as well as those of the interleukin-2 and interleukin-2 receptor genes. Transcriptional transactivation of lymphocyte-specific genes by tat-l was thus implicated in the facilitation of T-cell transformation by HTLV-l. Molecular analyses of the genetic regulation of expression of the human immunodeficiency virus (HIV) (the etiologic agent of acquired immunodeficiency syndrome) delineated the genomic location and structure of two previously unidentified viral genes referred to as tat-III and trs. Both of these genes are shown to be essential for HIV replication. Tat-III appears to act by enhancing the ability of viral mRNAs to be efficiently translated, while trs controls the relative distribution of viral mRNA species synthesized in the course of an infection. The evaluation of the mechanism of cytopathogenesis by HIV demonstrated that the specific interaction between the viral envelope glycoprotein and the CD4 T-cell surface molecule plays a major role in virally induced T-cell killing. (Full text available from University Microfilms International, Ann Arbor, MI, as Order No: AAD87-07661)

Keywords: Gene Expression Regulation Human HIV/*GENETICS HTLV-BLV Viruses/*GENETICS Transcription Factors/*GENETICS *Transcription, Genetic Translation, Genetic THESIS

880330
M8830439

AEGiS is a 501(c)3, not-for-profit, tax-exempt, educational corporation. AEGiS is made possible through unrestricted funding from Boehringer Ingelheim, Bridgestone/Firestone Charitable Trust, Bristol-Myers Squibb Company, Elton John AIDS Foundation, Gill Foundation, the National Library of Medicine, Quest Diagnostics, Roche and Trimeris, and donations from users like you. Always watch for outdated information. This article first appeared in 1988. This material is designed to support, not replace, the relationship that exists between you and your doctor.

AEGiS presents published material, reprinted with permission and neither endorses nor opposes any material. All information contained on this website, including information relating to health conditions, products, and treatments, is for informational purposes only. It is often presented in summary or aggregate form. It is not meant to be a substitute for the advice provided by your own physician or other medical professionals. Always discuss treatment options with a doctor who specializes in treating HIV.

Copyright ©1980, 1988. AEGiS. All materials appearing on AEGiS are protected by copyright as a collective work or compilation under U.S. copyright and other laws and are the property of AEGiS, or the party credited as the provider of the content. .