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The Herpesviruses: Volume 3

ISBN-13: 9781461294566 / Angielski / Miękka / 2011 / 432 str.

Bernard Roizman
The Herpesviruses: Volume 3 Roizman, Bernard 9781461294566 Springer - książkaWidoczna okładka, to zdjęcie poglądowe, a rzeczywista szata graficzna może różnić się od prezentowanej.

The Herpesviruses: Volume 3

ISBN-13: 9781461294566 / Angielski / Miękka / 2011 / 432 str.

Bernard Roizman
cena 201,72
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A great truth is a truth whose opposite. is also a great truth. Thomas Mann (Essay on Freud, 1937) This volume centers on pseudorabies (PR V), herpes simplex viruses 1 and 2 (HSV-1 and HSV-2), and human cytomegalovirus (CMV) and fulfills three objectives. The chapters on the epidemiology and latency of HSV, and on the glycoproteins specified by HSV and CMV, set the stage for the discussions of the immunobiology and pathogenesis of human herpesvirus infections in Volume 4. The epidemiology of HSV is the basis of our understanding of the spread and survival of this virus in the human populations. Central to the epidemiology of HSV and its pathogenesis in humans is the ability of the virus to remain in a latent state for the life of its host. The viral membrane glycoproteins are among the most interesting virion proteins, primarily because of their critical role in the initiation of infection. Since they are the surface membrane proteins of the virion and appear on the surface of productively infected cells, they are also the obvious if not the exclusive targets of the immune response. The chapters on the transforming potential of HSV and CMV, and on the role of HSV in human cancer, deal with challenging problems requiring rather different experimental tools.

Kategorie:
Nauka, Medycyna
Kategorie BISAC:
Science > Botanika
Medical > Choroby zakaźne
Science > Mikrobiologia
Wydawca:
Springer
Seria wydawnicza:
Viruses
Język:
Angielski
ISBN-13:
9781461294566
Rok wydania:
2011
Wydanie:
Softcover Repri
Numer serii:
000076407
Ilość stron:
432
Waga:
0.82 kg
Wymiary:
25.4 x 17.8
Oprawa:
Miękka
Wolumenów:
01
Dodatkowe informacje:
Wydanie ilustrowane

1 Epidemiology of Herpes Simplex Viruses.- I. Introduction.- II. Historical Background.- III. Descriptive Epidemiology.- A. Epidemiology of HSV-1.- B. Epidemiology of Genital HSV Infections.- C. Treatment of Primary Infections.- IV. Recurrent Infection versus Reinfection with HSV.- A. Latency.- B. Recurrent HSV-1 Infections.- C. Therapy of Recurrent HSV-1 Infections.- D. Recurrent HSV-2 Infections.- E. Therapy of Recurrent HSV-2 Infections.- V. Diseases of Epidemiologic Importance.- A. Herpes Keratoconjunctivitis.- B. Skin Infection.- C. Infections of the Immunocompromised Host.- D. Infections of the Newborn.- E. Infection of the Nervous System.- F. Other Neurologic Syndromes.- G. Unusual Outbreaks of Infection.- VI. HSV Infections and Cervical Carcinoma.- A. General Association.- B. Epidemiology of Cervical Carcinoma.- C. Molecular Epidemiology of HSV-2 Antigens in Cervical Carcinoma.- VII. Conclusion.- References.- 2 Individual HSV Transcripts: Characterization of Specific Genes.- I. Introduction.- II. HSV mRNA.- A. General Properties.- B. Nuclear Forms of HSV mRNA.- III. RNA Expressed in the Infected Cell.- A. Temporal Regulation of HSV Gene Expression.- B. Effect of HSV Infection on Host Cell RNA.- C. Gross Localization of HSV Transcripts.- IV. Detailed Analysis of Specific HSV Transcripts.- A. Isolation, Localization, and Translation of Specific HSV-1 mRNA Species.- B. High-Resolution Mapping of HSV-1 mRNA.- V. Specific HSV Genes.- A. Corelation of HSV Biological Markers with Specific mRNAs.- B. ? Genes.- C. HSV DNA Replication Machinery.- D. HSV Glycoproteins.- E. Structural Proteins.- F. Genes Involved with Morphological Transformation.- G. HSV Gene Expression during Latency.- VI. A Typical HSV-1 Transcription Unit.- A. Control Regions.- B. HSV Control Regions as Eukaryotic Promoters.- C. Properties of “Typical” HSV Structural Genes.- D. Transcription Termination.- VII. Generation of HSV Transcript ‘Families’.- A. Multiple Promoters.- B. Inefficient Termination.- C. Interior Promoters.- D. Splicing.- E. Do the Proteins Encoded by Overlapping HSV mRNA Families Have Related Functions?.- References.- 3 Molecular Biology of Pseudorabies Virus.- I. Introduction.- II. Morphology.- III. Stability in the Presence of Physical and Chemical Agents.- IV. Virus Proteins.- A. Structural Protein Components.- B. Virus Neutralization.- C. Antigenic Relationship between PRV and Some Other Herpesviruses.- V. Virus Genome.- A. Size and Base Composition.- B. Genome Structure.- C. Restriction Enzyme Cleavage Maps.- D. Functional Identity of the Two Isomeric Forms of PRVDNA.- E. Strain Variability.- F. Genomes of Vaccine Strains.- VI. Virus Replication in Cell Culture.- A. Virus Growth Cycle.- B. Cytopathic Effects on Cells in Culture.- C. Host Range.- VII. RNA Synthesis in PRV-Infected Cells.- A. Patterns of Transcription of the Virus Genome.- B. Transition from IE RNA to Early RNA Transcription.- C. Transition from Early to Late RNA Transcription.- D. Characteristics of Virus Transcripts.- E. Accumulation of Virus mRNAs in the Infected Cells.- VIII. Protein Synthesis in the Infected Cells.- A. Patterns of Virus Protein Synthesis.- B. Mapping of Virus Polypeptides.- C. Control of Virus Protein Synthesis.- D. Functions of Some Nonstructural Virus Proteins.- IX. DNA Synthesis in PRV-Infected Cells.- A. Rate of Virus DNA Synthesis.- B. Properties of Intracellular Virus DNA.- X. Origins of DNA Replication.- XI. Mode of PRV DNA Replication.- XII. Maintenance of Sequence Identity of the Inverted Repeats.- XIII. Isomerization of the Virus Genome.- XIV. Process of Virion Assembly.- A. Capsid Assembly.- B. Precursor Relationship between Empty Capsids and Nucleocapsids.- C. Cleavage of Concatemeric DNA and Nucleocapsid Formation.- D. Biogenesis of the Virus Membrane.- XV. Organization of the Genome of PRV.- A. Phenotypie Characterization of Mutants.- B. The Genetic Map.- XVI. Cellular Macromolecular Synthesis in the Infected Cells.- A. Protein Synthesis.- B. RNA Synthesis.- C. DNA Synthesis.- XVII. Sequence Homology between the Genomes of PRV and HSV.- XVIII. Aujeszky’s Disease.- References.- 4 Herpes Simplex Virus Latency.- I. Introduction.- A. Development of the Concept of Latent Infection.- B. Neurotropism of HSV and Animal Models.- II. The Site of Latent Infection.- A. Neural Sites.- B. Extraneural Sites.- III. Establishment of Latent Infection in Ganglia.- A. Introduction.- B. Spread of Virus from the Periphery.- C. Events in the Peripheral Tissue during Primary Infection.- D. The Latently Infected Cell.- E. Viral Functions Associated with the Establishment and Maintenance of Latency in Neurons.- F. The State of Latency: Presence and Expression of Viral Functions in the Latently Infected Ganglion.- IV. Reactivation of the Latent Infection and the Production of Recurrent Disease.- A. Introduction.- B. Mechanisms Underlying the Reactivation from Latency.- C. Events That May Result from Reactivation of Latency.- V. Evolutionary Aspects of Latency.- References.- 5 Herpes Simplex Viruses and Their Roles in Human Cancer.- I. Introduction.- II. Definition of Risk.- A. Theoretical Considerations.- B. Risk Estimates from Epidemiologic Studies.- III. Viral Genetic Information in Cancer Cells.- A. HSV Antigens Expressed in Cancer Cells.- B. HSV DNA Sequences in Cancer Cells.- IV. Comments.- References.- 6 Transforming Potential of Herpes Simplex Viruses and Human Cytomegalovirus.- I. Introduction.- II. Transforming Potential of HSV.- A. Morphological Transformation of Cells in Culture by HSV-1 and HSV-2 Virions.- B. Frequency of Transformation.- C. Association of Viral DNA Sequences with Transformation.- D. Transformation of Cells in Culture by Genomic Fragments of HSV-1.- E. Transformation of Cells in Culture by Genomic Fragments of HSV-2.- F. Homologies among mtr-I and mtr-II of the HSV-1 and HSV-2 Genomes.- G. Mechanisms of Transformation by HSV.- III. Transforming Potential of HCMV.- A. Morphological Transformation of Cells in Culture by HCMV.- B. Transformation by HCMV DNA and DNA Fragments.- IV. Conclusion.- References.- 7 Glycoproteins Specified by Herpes Simplex Virus.- I. Introduction.- II. The HSV Glycoproteins and Their Structural Genes.- A. Genetic Loci Encoding Glycoproteins.- B. Structures of the Glycoproteins.- C. Intermolecular Interactions.- III. Synthesis and Processing of the Glycoproteins.- A. Kinetics of Polypeptide Synthesis.- B. Regulation of Polypeptide Synthesis.- C. Sequence of Events and Intracellular Locations for Polypeptide Synthesis and Processing.- IV. Activities and Roles of the Glycoproteins.- A. Virion Infectivity.- B. Envelopment of Virions and Their Egress from Infected Cells.- C. Expression of Receptors for the Fc Region of IgG and for the C3b Component of Complement.- D. Cell Fusion.- E. Functional Relatedness of the HSV-1 and HSV-2 Glycoproteins.- V. Appendix.- References.- 8 Processing of the Oligosaccharide Chains of Herpes Simplex Virus Type 1 Glycoproteins.- I. Introduction.- II. HSV-1 Glycoproteins.- III. Biosynthesis and Characterization of the Oligosaccharide Chains of HSV-1 Glycoproteins.- A. General Pathway of Viral Glycoprotein Synthesis.- B. Assembly of N-Linlced Oligosaccharides in Precursors and in Mature Forms.- C. Relationship between N- and O-Glycosylation.- D. Glycans of pgC and gC.- E. Host-Cell Dependence of Glycosylation.- F. Benzhydrazone, an Inhibitor of HSV-1 Glycosylation.- IV. Relationship between Glyean Structure and Expression of HSV-1 Functions.- A. Yield of Infectious Virus.- B. Virion Egress.- C. Virus-Induced Cell Fusion.- References.- 9 Glycoproteins Specified by Human Cytomegalovirus.- I. Introduction.- II. CMV Glycoproteins f.- A. Glycoprotein Synthesis in Infected Cells.- B. Glycoproteins in the Plasma Membrane, Dense Bodies, and Virions.- III. Characterization of CMV Glycoproteins with Monoclonal Antibodies.- A. Monoclonal Antibodies to CMV.- B. Characterization of Antigenically Distinct Glycoproteins.- C. Purification of Glycoproteins on Monoclonal Antibody Affinity Columns.- IV. Mapping CMV Genes.- V. Synthesis and Processing of CMV gA.- A. Polymorphism of gA.- B. Concluding Remarks.- References.



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