Abstract
Picornavirus infection is characterised by host cell shutoff, wherein host transcription and translation processes are severely impaired. Picornavirus proteins interact with host cell proteins, resulting in alterations in the host cell synthetic, signalling and secretory machinery, and facilitating transcription and translation of viral proteins to achieve increased virus replication and assembly. Among the many cellular pathways affected, recent studies have shown that disruption of nucleocytoplasmic trafficking via inhibition of the functions of the nuclear pore may be a common means of picornavirus- induced pathogenesis. Disruption of nuclear pore functions results in nuclear proteins being relocalised to the cytoplasm and reduced export of RNA, and may be a mechanism by which picornaviruses evade host cell defences such as interferon signalling, by blocking signal transduction across the nuclear membrane. However, the mechanisms used and the viral proteins responsible differ between different genera and even between viruses in the same genus. This review aims to summarise current understanding of the mechanisms used by picornaviruses to disrupt host cell nucleocytoplasmic trafficking.
Keywords: Picornavirus, rhinovirus, poliovirus, cardiovirus, nucleocytoplasmic trafficking, nucleoporins, virus replication and assembly, picornavirus- induced pathogenesis, interferon signalling, poliovirus (PV)
Infectious Disorders - Drug Targets
Title: Modulation of Host Cell Nucleocytoplasmic Trafficking During Picornavirus Infection
Volume: 12 Issue: 1
Author(s): Parisa Younessi, David A. Jans and Reena Ghildyal
Affiliation:
Keywords: Picornavirus, rhinovirus, poliovirus, cardiovirus, nucleocytoplasmic trafficking, nucleoporins, virus replication and assembly, picornavirus- induced pathogenesis, interferon signalling, poliovirus (PV)
Abstract: Picornavirus infection is characterised by host cell shutoff, wherein host transcription and translation processes are severely impaired. Picornavirus proteins interact with host cell proteins, resulting in alterations in the host cell synthetic, signalling and secretory machinery, and facilitating transcription and translation of viral proteins to achieve increased virus replication and assembly. Among the many cellular pathways affected, recent studies have shown that disruption of nucleocytoplasmic trafficking via inhibition of the functions of the nuclear pore may be a common means of picornavirus- induced pathogenesis. Disruption of nuclear pore functions results in nuclear proteins being relocalised to the cytoplasm and reduced export of RNA, and may be a mechanism by which picornaviruses evade host cell defences such as interferon signalling, by blocking signal transduction across the nuclear membrane. However, the mechanisms used and the viral proteins responsible differ between different genera and even between viruses in the same genus. This review aims to summarise current understanding of the mechanisms used by picornaviruses to disrupt host cell nucleocytoplasmic trafficking.
Export Options
About this article
Cite this article as:
Younessi Parisa, A. Jans David and Ghildyal Reena, Modulation of Host Cell Nucleocytoplasmic Trafficking During Picornavirus Infection, Infectious Disorders - Drug Targets 2012; 12 (1) . https://dx.doi.org/10.2174/187152612798994993
DOI https://dx.doi.org/10.2174/187152612798994993 |
Print ISSN 1871-5265 |
Publisher Name Bentham Science Publisher |
Online ISSN 2212-3989 |
- Author Guidelines
- Graphical Abstracts
- Fabricating and Stating False Information
- Research Misconduct
- Post Publication Discussions and Corrections
- Publishing Ethics and Rectitude
- Increase Visibility of Your Article
- Archiving Policies
- Peer Review Workflow
- Order Your Article Before Print
- Promote Your Article
- Manuscript Transfer Facility
- Editorial Policies
- Allegations from Whistleblowers
- Announcements
Related Articles
-
Promises of Nanotechnology for Drug Delivery to Brain in Neurodegenerative Diseases
Current Nanoscience Therapeutic Targeting of Epigenetic Components in Amyotrophic Lateral Sclerosis (ALS)
Current Medicinal Chemistry Morphofunctional Aspects of the Blood-Brain Barrier
Current Drug Metabolism Gender Hormones: Role in the Pathogenesis of Central Nervous System Disease and Demyelination
Current Neurovascular Research Current Landscape of Natural Products against Coronaviruses: Perspectives in COVID-19 Treatment and Anti-viral Mechanism
Current Pharmaceutical Design Advances in Design and Development of Inhibitors of Nitric Oxide Synthases
Current Enzyme Inhibition How to Get from Here to There: Macrophage Recruitment in Alzheimers Disease
Current Alzheimer Research Hematopoietic Stem Cell Transplantation for the Treatment of Autoimmunity in Type 1 Diabetes
Current Stem Cell Research & Therapy VIP in Neurological Diseases: More Than A Neuropeptide
Endocrine, Metabolic & Immune Disorders - Drug Targets Telomeres, Senescence and Longevity: The Role of Oxidative Stress and Antioxidants
Current Pharmacogenomics Towards Retinoid Therapy for Alzheimers Disease
Current Alzheimer Research Lysosomal Storage Diseases and the Blood-Brain Barrier
Current Pharmaceutical Design The Leptin System: A Potential Target for Sepsis Induced Immune Suppression
Endocrine, Metabolic & Immune Disorders - Drug Targets Advances in Interleukin-12 Gene Therapy for Acquired Liver Diseases
Current Gene Therapy The Use of Statins in Respiratory Diseases
Current Respiratory Medicine Reviews Anti-inflammatory and Immune Therapy for Alzheimers Disease: Current Status and Future Directions
Current Neuropharmacology Fibroblast Growth Factors, Fibroblast Growth Factor Receptors, Diseases, and Drugs
Recent Patents on Cardiovascular Drug Discovery The Role of Growth Factors in the Prevention and Treatment of Chemotherapy-Induced Peripheral Neurotoxicity
Current Drug Safety Identification of Essential cis Element in 5'UTR of Nef mRNA for Nef Translation
Current HIV Research Monoamine Involvement in the Antidepressant-Like Effect of β-Caryophyllene
CNS & Neurological Disorders - Drug Targets