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Hormones, regulators and viruses /

Vitamins and Hormones series, highlights new advances in the field, with this new volume presenting interesting chapters.Each chapter is written by an international board of authors- Provides the authority and expertise of leading contributors from an international board of authors- Presents the lat...

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Bibliographic Details
Corporate Author: ScienceDirect (Online service)
Other Authors: Litwack, Gerald (Editor)
Format: eBook
Language:English
Published: Cambridge, MA : Academic Press, 2021.
Series:Vitamins and hormones ; v. 117.
Subjects:
Hormones.
Viruses.
Stem cells.
Hormones
Viruses
Stem Cells
Virus.
Cellules souches.
hormone.
Stem cells
Electronic books.
Online Access:Connect to the full text of this electronic book
Table of Contents:
  • Intro
  • Hormones, Regulators and Viruses
  • Copyright
  • Former Editors
  • Contents
  • Contributors
  • Preface
  • Chapter One: The interplay between the immune system and viruses
  • 1. Viral immune detection
  • 1.1. Pattern recognition receptors (PRRs)
  • 2. Toll like receptors (TLRs)
  • 3. TLR signaling pathways
  • 4. RIG-I-like receptors (RLRs)
  • 5. NOD-like receptors (NLRs)
  • 6. Anti-viral IFNs
  • 6.1. IFN stimulated genes (ISGs)
  • 6.2. Regulation of IFN signaling
  • 6.3. Phosphorylation
  • 6.4. SOCS proteins
  • 7. Viral evasion of the IFN response
  • References
  • Chapter Two: Strategies to identify and develop antiviral peptides
  • 1. Strategies to identify and develop antiviral peptides
  • 1.1. Peptide libraries
  • 1.1.1. Phage display libraries
  • 1.1.2. Synthetic peptide libraries
  • 1.2. Peptide microarrays
  • 1.3. Computer-aided in silico peptide libraries
  • 1.4. Deep machine learning
  • 1.4.1. AntiVPP 1.0
  • 1.4.2. StraPep
  • 1.4.3. CRDD-AVPdb
  • 2. Antiviral peptides against viruses
  • 2.1. Peptides from animal/insect origin
  • 2.2. Milk protein peptides
  • 2.3. Host defensive peptides
  • 2.4. Enfuvirtide and derivatives
  • 2.5. Anti-heparin sulfate peptides
  • 2.6. Synthetic peptides
  • 3. Advantages of peptides
  • 4. Limitations of peptides
  • 4.1. Chemical modifications to overcome limitations
  • 5. Delivery of peptides using nanotechnology
  • 5.1. Potential translation of nano carrier-based antiviral peptides to clinical application
  • 6. Conclusion
  • Acknowledgments
  • Disclosure of interest
  • References
  • Chapter Three: Cell-penetrating peptides in the intracellular delivery of viral nanoparticles
  • 1. Virus-derived CPPs
  • 1.1. Characterization of virus-derived CPPs
  • 1.2. CPPs derived from structural viral proteins
  • 1.3. CPPs derived from nonstructural viral proteins
  • 1.4. Nucleic acid binding properties.
  • 3.1. Stress increases the incidence of HSV-1 reactivation from latency
  • 3.2. GCs rapidly induce BoHV-1 reactivation from latency by stimulating viral and cellular gene expression in TG sensory ...
  • 3.3. Regulation of productive infection by stress and GR
  • 4. Promoters that drive key viral regulatory genes are stimulated by GR and specific stress-induced transcription factors
  • 4.1. Reactivation from latency is stimulated by key viral regulatory proteins
  • 4.2. ICP0 promoter is transactivated by stress-induced transcription factors
  • 4.3. The ICP4 promoter is transactivated by stress-induced transcription factors
  • 4.4. Activation of BoHV-1 promoters by GR and stress-induced transcription factors
  • 5. Summary and conclusions
  • Acknowledgments
  • References
  • Chapter Six: Cholesterol: A key player in membrane fusion that modulates the efficacy of fusion inhibitor peptides
  • 1. Cholesterol: An important constituent of the cell membrane
  • 2. Effect of cholesterol on membrane organization dynamics
  • 3. Effect of cholesterol on viral entry
  • 3.1. Effect of cholesterol on entry of virus containing class I fusion protein
  • 3.1.1. Cholesterol and HIV entry
  • 3.1.2. Cholesterol and influenza virus entry
  • 3.1.3. Cholesterol and paramyxovirus entry
  • 3.1.4. Cholesterol and severe acute respiratory syndrome coronavirus (SARS-CoV) entry
  • 3.2. Effect of cholesterol on entry of virus containing class II fusion protein
  • 3.2.1. Cholesterol and flavivirus entry
  • 3.2.2. Cholesterol and alphavirus entry
  • 3.3. Effect of cholesterol on entry of virus containing class III fusion protein
  • 3.3.1. Cholesterol and VSV entry
  • 4. Effect of cholesterol on organization and dynamics of fusion peptide: Implication in membrane fusion
  • 4.1. Effect of cholesterol on HIV gp41 fusion peptide
  • 4.2. Effect of cholesterol on SARS-CoV fusion peptide.
  • 5. Effect of cholesterol on peptide-based fusion inhibitor
  • 6. Concluding remark and future perspectives
  • Acknowledgments
  • Conflict of interest
  • References
  • Chapter Seven: Immunoinformatics aided design of peptide-based vaccines against ebolaviruses
  • 1. Introduction
  • 2. Methodology
  • 2.1. Retrieval of viral protein sequences
  • 2.2. Determination of conserved peptide sequences
  • 2.3. Prediction of peptides containing CD8 T cell epitopes
  • 2.4. B-cell epitope prediction
  • 2.5. Screening peptides for undesirable responses
  • 2.6. Peptide-HLA interaction
  • 2.6.1. HLA coverage analysis
  • 2.6.2. Population coverage analysis
  • 2.6.3. Molecular docking
  • 2.6.3.1. AutoDock Vina
  • 2.6.3.2. CABS-dock
  • 3. An example from a study applying described methodology
  • 4. Conclusion
  • Acknowledgment
  • References
  • Chapter Eight: Hormonal regulation and functional role of the ``renal´´ tubules in the disease vector, Aedes aegypti
  • 1. The mosquito, Aedes aegypti
  • 1.1. A. aegypti as a disease vector
  • 1.2. A. aegypti lifecycle and distribution
  • 1.3. A. aegypti excretory system
  • 2. The role of MTs
  • 2.1. The cellular composition of MTs in A. aegypti
  • 2.2. Ion transport in stimulated A. aegypti MTs
  • 3. Neuroendocrine regulation of the MTs
  • 3.1. The neuroendocrine system of A. aegypti
  • 3.2. Hormonal regulation of MTs
  • 4. Conclusions and future directions
  • Acknowledgments
  • References
  • Chapter Nine: Inhibition of hepatitis C virus by vitamin D
  • 1. Vitamin D supplementation of interferon-based therapy
  • 2. Molecular mechanism underlying the anti-HCV effect of vitamin D3
  • 2.1. Antiviral effect of vitamin D3 on HCV
  • 2.2. Antiviral effect of 25-(OH)D3 on HCV
  • 2.2.1. Anti-HCV effect of 25-(OH)D3
  • 2.2.2. Resistance mutation induced by 25-(OH)D3 treatment
  • 2.2.3. Mechanism underlying the anti-HCV effect of 25-(OH)D3.