HIV-I : molecular biology and pathogenesis : clinical applications /
Although it is one of the most-widely studied viruses, many mysteries still remain about HIV. Covering the latest advances and challenges associated with clinical application of new antiviral drugs and vaccines, this revised edition is a companion to Murad:HIV-1: Molecular Biology and Pathogenesis,...
| Otros Autores: | , , |
|---|---|
| Formato: | eBook |
| Lenguaje: | English |
| Publicado: |
Amsterdam ; Boston :
Elsevier/Academic Press,
2008.
|
| Edición: | 2nd ed. / |
| Colección: | Advances in pharmacology ;
vol. 56. |
| Materias: | |
| Acceso en línea: | https://sciencedirect.proxyucr.elogim.com/bookseries/advances-in-pharmacology/vol/56/suppl/C |
Tabla de Contenidos:
- Front Cover; HIV-1: Molecular Biology and Pathogenesis; Copyright Page; Contents; Contributors; Preface written by Robin A. Weiss; A. HIV Types (HIV-1 and HIV-2); B. Genotype Classification of HIV-1s; C. HIV-2: Genotype Classification and Geographic Distribution; A. Global HIV-1 Variability; B. HIV-1 Variants in Asia; C. Other HIV-1 Variants of Geographical Relevance; D. Emergence og HIV-1 Recombinants Worldwide; A. Phylogenetic Sequeuce Analysis; B. Alternative Methods (Heteroduplex Mobility Assay and Serotyping); VI. Origin of HIVs and Genesis of HIV-1 Pandemic.
- A. HIV/AIDS as a ""Zoonosis""B. Dating the Origin of Pandemic HIV-1 Strains; A. HIV-1 Subtypes and Disease Progression; B. HIV-1 Dual Infection, Superinfection, and Recombination; C. Biological Implications of Recombination; Acknowledgments; References; B. Nonnucleoside Reverse Transcriptase Inhibitors; C. Protease Inhibitors; A. Initiation of Therapy; B. Initial Regimen; C. Long-Term Management; D. Resistance; E. Drugs in Development; IV. Conclusion; References; A. Protective Role of HIV-1-Specific T-Cell Responses; B. Kinetics of HIV-1-Specific T-Cell Responses in Primary Infection.
- C. Phenotypic and Functional Profiles of HIV-1-Specific CD4 and CD8 T-Cell ResponsesD. Phenotype; E. Function; F. Specificity and Breadth of HIV-1-Specific T-Cell Responses; References; II. Background; III. Inhibition of Viral Attachment; A. gp120 Inhibitors; B. Targeting CD4; IV. Chemokine Receptors in HIV Infection; V. Targeting Coreceptor Binding; A. CXCR4 Inhibition; B. Targeting CCR5 for HIV Therapy; VI. Fusion Inhibitors; A. Targeting gp41; B. Inhibition of Membrane Fusion; VII. Resistance to Inhibitors of Viral Entry; VIII. Use Entry Inhibitors as Microbicides; References.
- B. Mechanism of HIV-1 RT DNA Polymerase ActivityA. Mechanisms of NRTI Inhibition; B. NRTI Approved for Clinical Use; C. Investigational NRTI; D. HIV-1 Resistance to NRTIs; V. Nonnucleoside Reverse Transcriptase Inhibitors (NNRTIs); A. Mechanisms of NNRTI Inhibition; B. NNRTI Approved for Clinical Use; C. Investigational NNRTI; D. HIV-1 Resistance to NNRTIs; E. Interactions Between NNRTI and NRTI Resistance Mutations; F. Use of NNRTI as Microbicides; VI. Other Inhibitors of HIV-1 RT; A. Inhibitors of HIV-1 RT RNH; B. Inhibitors of HIV-1 RT Dimerization.
- C. Inhibitors of the Initiation of Reverse TranscriptionD. RT-Directed Mutagenic Inducers; VII. Conclusion; Acknowledgments; References; A. Mechanism of Action of PIs; B. Protease Structures and Substrate-Based Inhibitors; C. Design of Symmetry-Based Inhibitors; D. Structure-Based PIs; A. Emergence of Drug Resistance to PIs; B. Primary and Secondary Mutations; C. Active site Mutants; D. Nonactive Site Mutants; E. Cleavage Site Mutants; F. Noncleavage Site Mutants; G. Insertions in Gag-Pol Polyproteins; VII. PIs with Activity Against Drug-Resistant HIV-1.