Important note: Information in this article was accurate in 1987. The state of the art may have changed since the publication date.
GENOMIC VARIATION OF HTLV-III/LAV, THE RETROVIRUS OF AIDS
Banbury Rep; 22:235-47 1985. Unique Identifier : AIDSLINE ICDB/87632436 Hahn BH; Shaw GM; Wong-Staal F; Gallo RC; Lab. of Tumor Cell Biology, Div. of Cancer Treatment, NCI,; Bethesda, MD 20205
Abstract:
A novel human retrovirus, HTLV-III/LAV, with T-lymphotropic and cytopathic properties has been identified as the causative agent of the acquired immunodeficiency syndrome (AIDS). A body of evidence relevant to the issue of genome variation of HTLV-III/LAV is summarized. To define the nature and spectrum of variation among different viruses, 18 consecutive isolates of HTLV-III/LAV from patients with AIDS, AIDS-related complex, or no clinical disease were isolated by restriction enzyme mapping and Southern hybridization. An isolate from a Haitian man with AIDS was also molecularly cloned and sequenced, and compared to prototype HTLV-III/LAV isolates. This particular virus isolate, HTLV-IIIRF, was chosen for detailed analysis since it was derived from a restricted geographic region relatively early in the AIDS epidemic and preliminary analysis suggested that it was not closely related to other HTLV-III/LAV viruses. Results showed that a spectrum of variation, or diversity exists among the HTLV-III/LAV isolates. No two viral isolates were identical in their restriction enzyme maps but all hybridized throughout their genomes to a full-length, cloned probe derived from the prototype AIDS virus, HTLV-IIIB. Analysis of the HTLV-IIIRF genome confirmed that genomic diversity is a prominent feature of HTLV-III/LAV and that it is the envelope gene which varies most among different viral isolates. It was found that changes within the viral envelope are not uniform in distribution; instead, genomic changes cluster in the exterior portion of the envelope glycoprotein and coincide with regions that, based on their secondary structure, hydrophilicity, and glycosylation pattern, represent predicted antigenic sites. The implications of these findings with respect to the biology of HTLV-III/LAV, its evolution, and the development of diagnostic reagents and vaccines are discussed. (31 Refs)
Keywords: Acquired Immunodeficiency Syndrome/*MICROBIOLOGY Antigenic Determinants/GENETICS *Genes, Viral Glycoproteins/GENETICS/IMMUNOLOGY Human HIV/*GENETICS/IMMUNOLOGY Male Variation (Genetics) Viral Envelope Proteins/GENETICS/IMMUNOLOGY MEETING PAPER
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.
Important note: Information in this article was accurate in 1987. The state of the art may have changed since the publication date.
