E-Book, Englisch, 185 Seiten
Maramorosch / Shatkin / Murphy Advances in Virus Research
1. Auflage 2009
ISBN: 978-0-08-095087-7
Verlag: Elsevier Science & Techn.
Format: EPUB
Kopierschutz: 6 - ePub Watermark
E-Book, Englisch, 185 Seiten
ISBN: 978-0-08-095087-7
Verlag: Elsevier Science & Techn.
Format: EPUB
Kopierschutz: 6 - ePub Watermark
Published since 1953, Advances in Virus Research covers a diverse range of in-depth reviews providing a valuable overview of the current field of virology. The impact factor for 2007 is 3.120, placing it 9th in the highly competitive category of virology.
* Contributions from leading authorities * Informs and updates on all the latest developments in the field
Autoren/Hrsg.
Weitere Infos & Material
1;Front Cover;1
2;Advances in Virus Research;4
3;Copyright Page;5
4;Contents;6
5;Chapter 1: Looking Back in 2009 at the Dawning of Antiviral Therapy Now 50 Years Ago: An Historical Perspective;8
5.1;I. Introduction;10
5.2;II. Thiosemicarbazones: The First Antiviral Drugs Found Active Against the Poxvirus Vaccinia Virus;11
5.3;III. Renaissance of the Poxvirus Inhibitors: Antiviral Drugs Against a Bioterrorist Poxvirus (Variola Virus) Attack;13
5.4;IV. Benzimidazole Derivatives: Second Attempt to Launch the Antiviral Chemotherapy Era;15
5.5;V. Renaissance of the Benzimidazole Derivatives: Now Turning into Lead Candidates for the Treatment of Human CMV Infections;18
5.6;VI. 5-Substituted 2'-Deoxyuridines: Idoxuridine (IDU) and Trifluridine (TFT), the Third and Definitive Attempt to Unleash Antiviral Chemotherapy;20
5.7;VII. 5-Substituted 2'-Deoxyuridines: IDU (and TFT) as the Starting Point(s) for Other 5-Substituted 2'-Deoxyuridines, that is, BVDU [(E)-5-(2-Bromovinyl)-2'-Deoxyuridine];22
5.8;VIII. Arabinosyladenine (ara-A), Originally Conceived as an Antitumor Agent, the First Antiviral Drug Licensed and Used for Systemic Treatment;23
5.9;IX. Acyclovir: The Start of the Selective Antiviral Chemotherapy Era, and Still the ``Gold Standard´´ for HSV Therapy;25
5.10;X. Anti-influenza Virus Therapy: A First Attempt (DRB), Followed by a Second (Amantadine) and a Third Attempt (Neuraminidase Inhibitors);27
5.11;XI. Ribavirin and Interferon, Two ``Old-Timers´´, Joining Forces in the Treatment of a Relatively New Disease, Hepatitis C;29
5.12;XII. (S)-9-(2,3-Dihydroxypropyl)adenine (DHPA), the First Acyclic Adenosine Analog, Leading to S-Adenosylhomocysteine (SAH) Hydrol Inhibitors as Broad-Spectrum Antiviral Agents;30
5.13;XIII. (S)-9-(2,3-Dihydroxypropyl)adenine (DHPA) Leading to the First Acyclic Nucleoside Phosphonate, (S)-9-(3-hydroxy-2-phosphonylmethoxypropyl)Adenine (HPMPA), As a Broad-Spectrum Antiviral Agent;32
5.14;XIV. 9-(2-Phosphonylmethoxyethyl)adenine (PMEA), the Sister Compound of HPMPA;33
5.15;XV. From PMEA (Adefovir) to PMPA (tenofovir): It All Depends on the Substitution of a Methyl Group for a Hydrogen;35
5.16;XVI. Suramin, the First Antiviral Drug Ever Shown to Inhibit HIV Infection Both in vitro and in vivo;36
5.17;XVII. The Nucleoside Reverse Transcriptase Inhibitors (NRTIs) with Azidothymidine (AZT) as the Starting Point;37
5.18;XVIII. The Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTIs), with the HEPT and TIBO Derivatives as the Starting Point;39
5.19;XIX. The HIV Protease Inhibitors (PIs), Hailed From Their Inception, as Resulting from rational design;41
5.20;XX. New HIV Inhibitors, Targeted at Either Fusion (Enfuvirtide), Coreceptor usage (maraviroc), or Integrase (Raltegravir);47
5.21;XXI. Conclusion;49
5.22;Acknowledgment;50
5.23;References;50
6;Chapter 2: Use of Animal Models to Understand the Pandemic Potential of Highly Pathogenic Avian Influenza Viruses;62
6.1;I. Introduction;63
6.2;II. Influenza A Virus Subtypes and Host Range;64
6.3;III. Avian Influenza A Virus in Humans;67
6.4;IV. Use of the Mouse Model to Study Influenza Virus Pathogenesis;70
6.4.1;A. Mouse model for human influenza A virus pathogenesis;70
6.4.2;B. Mouse model for H5N1 virus pathogenesis;72
6.4.3;C. Mouse model for H7 virus pathogenesis;74
6.4.4;D. Gene knockout mice in the study of avian influenza;75
6.4.5;E. Tropism of avian influenza viruses;77
6.5;V. Use of the Ferret Model to Study Influenza Virus Pathogenesis;78
6.5.1;A. Ferret model for human influenza A virus pathogenesis;78
6.5.2;B. Ferret model for H5N1 virus pathogenesis;79
6.5.3;C. Ferret model for H7 virus pathogenesis;80
6.5.4;D. Transmissibility of avian influenza viruses;81
6.6;VI. Molecular Basis of Avian Influenza Pathogenesis;82
6.6.1;A. Hemagglutinin cleavage site;83
6.6.2;B. Surface glycoproteins (HA and NA);84
6.6.3;C. Polymerase complex;85
6.6.4;D. PB2 protein;86
6.6.5;E. PB1-F2 protein;88
6.6.6;F. NS1 protein;88
6.7;VII. Conclusions;89
6.8;Acknowledgments;91
6.9;References;91
7;Chapter 3: Virus Versus Host Cell Translation: Love and Hate Stories;106
7.1;I. Introduction;110
7.2;II. Regulation Prior to Translation;111
7.2.1;A. Editing;111
7.2.1.1;1. Editing by nucleotide modification;111
7.2.1.2;2. Editing by nucleotide addition;113
7.2.2;B. Splicing;115
7.2.3;C. Subgenomic RNA synthesis;117
7.3;III. Initiation of Translation;118
7.3.1;A. Cap-dependent initiation;118
7.3.2;B. Closed-loop model or circularization;119
7.3.3;C. VPg and initiation;122
7.3.4;D. IRES-directed initiation;123
7.3.5;E. Non-AUG initiation codons;126
7.3.6;F. Multiple reading frames;129
7.3.6.1;1. Leaky scanning;129
7.3.6.1.1;a. In-frame initiation;130
7.3.6.1.2;b. Overlapping ORFs;130
7.3.6.2;2. Reinitiation;132
7.3.6.3;3. Shunting;134
7.3.7;G. Modification of cell factors involved in initiation;135
7.3.7.1;1. Phosphorylation of eIF2alpha;136
7.3.7.2;2. Modification of eIF4E and 4E-BP;138
7.3.7.2.1;a. Dephosphorylation of eIF4E and of 4E-BP1;139
7.3.7.2.2;b. Phosphorylation of eIF4E and 4E-BP1;141
7.3.7.3;3. Modification of eIF4G;141
7.3.7.3.1;a. Cleavage of eIF4G;141
7.3.7.3.2;b. Phosphorylation of eIF4G;142
7.3.7.4;4. Cleavage of PABP;143
7.3.7.5;5. Substitution of PABP;143
7.3.7.6;6. Cleavage of PBCP2;144
7.4;IV. Elongation of Translation;144
7.4.1;A. Frameshift;144
7.4.2;B. Modification of elongation factors;147
7.5;V. Termination of Translation;148
7.5.1;A. Readthrough;148
7.5.2;B. Suppressor tRNAs;152
7.5.2.1;1. Suppressors of UAG/UAA codons;152
7.5.2.2;2. Suppressors of UGA codons;152
7.5.3;C. Binding of release factors;153
7.6;VI. Conclusions;153
7.7;Acknowledgments;154
7.8;References;154
8;Index;178




