The Papovaviridae
Kluwer Academic/Plenum Publishers (Verlag)
978-0-306-42308-6 (ISBN)
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It has been more than twenty years since the isolation of polyoma virus and SV40, and the reports that they could produce tumors in animals and transformation of cells in culture. What was startling was that these biologic properties are associated with viruses that contain genetic in- formation that is able to code for only five or six proteins. Since that time, investigations with these viruses have been in four principal areas. One major area of study has been on cells transformed by viruses that show altered growth properties and specify new viral and cellular proteins. Transformation studies have focused on the tumor (T) antigens that are specified by the virus and are required to initiate and to maintain the transformed state. Current studies on transformation are summarized in Chapter 4. The second broad area of investigation concerns replication of viruses during a lytic cycle of infection. T-antigens that are the hallmark of transformed cells are also expressed in cells that are lytically infected and are required for viral DNA replication and also function to alter rates of transcription of the early and late viral genes. Except for T-antigen, virus replication depends on the cellular enzymatic machinery and so the description of viral macromolecular synthesis has provided valuable insights into the cellular biosynthetic pathways. These studies are described in Chapters 1-3. The studies that have medical relevance concern JC and BK viruses and there is evidence of widespread exposure of human populations to these agents.
1 The Papovaviruses: General Properties of Polyoma and SV40.- I. Early Studies with Polyoma Virus.- II. Early Studies with SV40.- III. Virus Classification.- IV. Virion Structure.- V. Structure of the Viral DNA.- VI. Late Viral Proteins.- VII. Early Events in Papovavirus Infection.- VIII. Papovavirus Host-Range Restriction.- IX. Chromatin Structure.- X. Virus Assembly.- XI. Concluding Remarks.- References.- 2 Transcription of SV40 and Polyoma Virus and Its Regulation.- I. RNA Polymerase II—Its Structure and General Properties.- II. SV40 Early Transcription.- A. 5’ Ends of SV40 Early mRNAs.- B. Regulation of Early Transcription.- C. Late-Early RNAs.- D. Mechanism of the Early-Early to Late-Early Switch in RNA Synthesis.- E. DNA Sequences That Control Transcription from SV40 Early Promoters.- III. Polyoma Virus Early Gene Transcription.- A. Properties of the Transcripts.- B. Regulation of Polyoma Early Transcription by T Antigen.- C. Control Sequences of Polyoma Early Gene Transcription.- IV. SV40 Late Gene Transcription.- A. Location of the 5’ Start Sites of Late Transcription.- B. Factors Involved in Positioning the 5’ Ends of Transcripts.- C. Changes in the DNA within the Leader Cause a Change in the Start Sites for Transcription.- D. The Structure of the Leader Determines the Metabolic Fate of the Transcript.- E. The Relationship between Viral DNA Replication and Late Transcription.- F. The Role of the GC-Rich Domain in Regulating Late Transcription.- G. T Antigen Affects SV40 Late Transcription.- V. Polyoma Virus Late Transcription.- VI. SV40 Enhancer.- A. The Effect on Activation of the Distance Separating the Promoter and Enhancer.- B. Activation of the SV40 Late Promoter by Enhancer.- C. Cell-Type Specificity of the SV40 Enhancer.- D. Critical Sequences Needed for Enhancer Activity.- E. Factors That Interact with the SV40 Enhancer.- F. Mechanism of Enhancer Action.- VII. Polyoma Virus Enhancer.- VIII. Splicing of Viral Transcripts.- A. The Secondary Structure of Pre-mRNA Has a Role in Splice Site Selection.- IX. Termination of Transcription.- X. The Viral Chromosome.- A. Isolation of Nucleoprotein Complexes.- B. Structure of the Complexes.- C. Location and Extent of the Hypersensitive Region.- D. Genetic Determination of the Hypersensitive Region.- E. Proteins Binding to the Hypersensitive Region.- F. Transcription Complexes.- G. Role of Chromatin Structure in the Early to Late Switch.- References.- 3 Replication of SV40 and Polyoma Virus Chromosomes.- I. Introduction.- A. Significance of Papovavirus DNA Replication.- B. SV40 and PyV Chromosomes as Models for the Replication of Mammalian Chromosomes.- II. Large T-Antigen.- A. Summary.- B. Background.- C. Initiation of Viral and Cellular DNA Replication.- D. Posttranslational Modifications.- E. Structural Characteristics.- F. T-Ag Binding to Cellular and Viral DNA.- G. In Vitro Associated Enzyme Activities.- H. In Vivo Associated Activities.- I. Genetic Alterations That Define Domains Functional in Replication.- III. The DNA Replication Cycle.- A. Summary.- B. cis-Acting DNA Sequences Required for Replication (ori).- C. Cellular Factors That Control Replication.- D. Role of ori in Excision and Integration of Viral DNA.- E. Subcellular Systems for the Replication of Viral Chromosomes.- F. Replicating Intermediates.- G. Separation of Sibling DNA Molecules.- H. Termination of Replication.- I. Comparison of Viral and Cellular Replicons.- IV. DNA Synthesis at Replication Forks.- A. Summary.- B. Okazaki Fragments.- C. RNA Primers, DNA Primase, and DNA Synthesis.- D. Gap-Filling Step.- E. DNA Polymerase ?[C1C2].- F. Replication Proteins Associated with Viral Chromosomes.- G. Initiation of DNA Synthesis at Replication Forks.- H. Initiation of DNA Synthesis in the ori Region.- V. Chromatin Structure and Assembly at Replication Forks.- A. Summary.- B. Mature Viral Chromosomes.- C. Segregation of “Old” Histone Octamers.- D. Structure of Chromatin at Replication Forks.- VI. Concluding Perspective.- References.- 4 Transformation by SV40 and Polyoma.- I. Introduction.- II. Tumorigenicity by SV40 and Polyoma.- A. SV40.- B. Polyoma.- III. In Vitro Cell Transformation.- A. Properties of Transformed Cells Which Can Be Used for Selection.- B. Other Properties of Transformed Cells.- C. Permissivity and Transformation.- D. Expression of Viral Functions in Transformed Cells.- E. Subcellular Localization of Viral Proteins in Transformed Cells.- F. Tumor-Specific Transplantation Antigens.- G. Association of Cellular Proteins with Viral Proteins.- H. Stimulation of Cellular Gene Expression in Transformed Cells.- I. The State of the Viral Genome in Transformed Cells.- J. Virus Rescue and Viral Genome Excision from Transformed Cells.- K. Abortive versus Permanent Transformation.- L. Role of Polyoma Large T and Middle T Proteins.- M. Role of SV40 Large T Protein in Cellular Transformation.- N. Role of Small t Protein in Cellular Transformation.- O. Large T Protein and the Maintenance of Transformation in SV40- and Polyoma-Transformed Cells.- IV. Conclusion.- References.- 5 Studies with BK Virus and Monkey Lymphotropic Papovavirus.- I. BK Virus.- A. Natural History.- B. Molecular Biology.- C. Summary and Conclusions.- II. Lymphotropic Papovavirus.- A. Biology.- B. Biochemical Studies.- C. Summary and Conclusions.- References.- 6 The Biology and Molecular Biology of JC Virus.- I. Introduction.- II. Biological Characteristics.- A. Distribution and Natural History.- B. Host Range.- C. Hemagglutination.- D. Measurement of Virus and Antibodies.- E. Antigenic Characteristics.- III. Physical Properties.- A. JCV Genome.- B. Viral Proteins.- C. Heterogeneity of the Genome.- D. DNA Transfection.- IV. Oncogenicity.- A. Experimental Animals.- B. In Vitro Transformation.- V. Association with Disease.- References.- Appendix Annotated Nucleotide Sequences and Restriction Site Lists for Selected Papovavirus Strains Charles E. Buckler and Norman P. Salzman.- SV40.- Polyoma Virus (A2).- BK Virus (Dunlop).- BK Virus (MM).- JC Virus (Madl).
| Erscheint lt. Verlag | 31.10.1986 |
|---|---|
| Reihe/Serie | The Viruses |
| Zusatzinfo | 474 p. |
| Verlagsort | New York |
| Sprache | englisch |
| Gewicht | 980 g |
| Themenwelt | Medizin / Pharmazie ► Medizinische Fachgebiete |
| Studium ► Querschnittsbereiche ► Infektiologie / Immunologie | |
| ISBN-10 | 0-306-42308-1 / 0306423081 |
| ISBN-13 | 978-0-306-42308-6 / 9780306423086 |
| Zustand | Neuware |
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