Advances in Molecular Biology and Targeted Treatment for AIDS

Since the discovery of HIV-l as the etiologic agent of acquired immunodeficiency syndrome (AIDS) in the early 1980s, remarkable progress has been made in both the basic understanding of the biological processes leading to AIDS and an accelerated effort in finding new treatments. As is often the case in rapidly advancing fields, most of the scientific discussions are best handled in specialized groups. The effort to organize a meeting on advances in molecular biology and targeted treatment for AIDS was an experiment of sorts to gather experts in selected areas of overlapping interests where advances in basic biology and its application in the development of new drugs could be discussed. Of necessity, the scope of the meeting had to be limited to maintain a certain focus. Important areas of rapid development in AIDS research, such as the vaccine development, epidemiology, animal models, etc. , had to be left out for more specialized meetings. The result, from all accounts, appeared to be quite a successful gathering, which provided a forum for informal discussions among scientists from industry and academic institutions. A remarkable feature of the AIDS virus is its genetic complexity and how some of its seemingly "extra genes" manage to regulate the normal functions of the host and most importantly its immune system.

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Proceedings of the Xth International Washington Spring Symposium at the George Washington University in Washington, D.C., held May 15-18, 1990.

Contenu
Viral DNA Replication and Integration.- Mechanistic Analysis of HIV-1 Reverse Transcriptase.- Analyses of HIV Integration Components.- DNA Cleaving Activity of Purified Human Immunodeficiency Virus Integration Protein.- A Thermodynamic Analysis of the Binding of Nucleic Acid to HIV-1 Reverse Transcriptase.- Rous Sarcoma Virus gag Gene Sequences Affect Viral RNA Splicing and Stability.- Ribonuclease H and Primer tRNA Binding Activities of HIV Reverse Transcriptase as Therapeutic Targets.- Role of Viral Regulatory Genes.- Human-Specific Factors Are Required for Tat-Mediated Trans-Activation of the HIV-1 and HIV-2 LTRs.- Role of the TAR Element in Regulating HIV Gene Expression.- Regulation of HIV-1 Gene Expression by the Tat Protein and the TAR Region.- HIV-1 Tat: A Transcriptional Activator that Recognizes a Structured RNA Target.- HIV-1 Tat Trans-Activates in the Absence of Its Target.- Trans-Activation Requires the Binding of the HIV-1 tat Protein to TAR RNA.- The HIV-1 tat Transactivator Contains an Arginine-Glycine-Aspartyl (RGD) Cell Adhesion Site.- Inhibition of HIV-1 Replication by Mutant Tat Peptides.- RNA-Protein Interactions Required for Rev Mediated Regulation of HIV Gene Expression.- A 5? Splice Site Is Essential for Rev and Rex Regulation of HIV Envelope Protein mRNA Expression.- Molecular Functional Studies of HIV-1 REV and NEF Proteins.- Structure and Function of HIV & SIV Nef Proteins.- Functional Analysis of the HIV-1 Gene Products vif and vpu.- Envelope Structure.- Envelope Pseudotypes of HIV and HTLV.- CD4-Pseudomonas Exotoxin: A Strategy for AIDS Therapy Based on Selective Killing of HIV-Infected Cells.- Binding of a Reduced-Peptide Inhibitor and a Statine-Containing Inhibitor to the Protease from the Human Immunodeficiency Virus.- A T Cell Clonewhich Reflects the Functional Defects Observed in the T Cells of AIDS Patients.- Roles of Nucleocapsid Cysteine Arrays in Retroviral Assembly and Replication: Possible Mechanisms in RNA Encapsidation.- Regulated Proteolytic Processing within Mature Retroviral Capsids.- Red Blood Cells Exposing CD4, As Competitive Inhibitors of HIV-1 Infection.- Antivirals and Gene Therapy.- Gene Therapy for AIDS.- Discovery of a Novel Potent Inhibitor of HIV Infection.- Antiretroviral Activity of Carbocyclic Nucleosides and Potential Use of Inosinate Dehydrogenase Inhibitors.- Lipophilic 6-Halo-2?,3?-Dideoxypurine Nucleosides: Potential Antiretroviral Agents Targeting HIVAssociated Neurologic Disorders.- Antiviral Evaluation of HIV-1 Specific Ribozyme Expressed in CD4+ HeLa Cells.- Resistance of Influenza A Viruses to Amantadine and Rimantadine.