Journal of Cell Science and Mutations

All submissions of the EM system will be redirected to Online Manuscript Submission System. Authors are requested to submit articles directly to Online Manuscript Submission System of respective journal.
Journal of Cell Science and Mutations 44 7897 074717

Scholarly Journals In Cellular Trafficking

Scholarly journals refers to the work done during the screening of submitted manuscripts and funding applications. This process encourages authors to meet the accepted standards of their discipline and reduces the dissemination of irrelevant findings, unwarranted claims, unacceptable interpretations, and personal views. Publications that have not undergone peer review are likely to be regarded with suspicion by academic scholars and professionals. Successful viral infection depends on the virus’ capacity to evade the host’s interferon (IFN)-mediated innate immune response, and thereby prevent the establishment in cells of an antiviral state. Viral evasion of IFN immunity is mediated by multifunctional, virus-encoded IFN-antagonist proteins, which interact with diverse host factors, including intracellular signalling and effector molecules of the IFN system; thus, IFN-antagonists represent potential targets for antiviral therapies, but the molecular events underlying their functions are currently poorly defined.Using live-cell imaging, molecular/cell biology and reverse genetics approaches with animal infection models, we have investigated the functions of the archetypal IFN-antagonist, rabies virus P protein, finding that it undergoes intricately regulated subcellular trafficking involving numerous sequences for interaction with the host cell’s nuclear transport machinery, cytoskeletal components, and IFN signalling/effector molecules. Through these interactions, P-protein undergoes highly regulated nucleocytoplasmic trafficking to target host factors in specific subcellular sites, and thereby regulate the trafficking/functions of components of the IFN system by several novel mechanisms. Our in vivo studies have shown that P-protein trafficking is a vital component of immune evasion and pathogenicity, the first such demonstration for any virus; importantly we found that mutations affecting P-protein interactions with cellular trafficking machinery can specifically attenuate virus in vivo. This work identifies IFN-antagonist subcellular trafficking/interactions as vital components in virulence, and potential therapeutic targets. IFN-antagonist trafficking has been reported for numerous human pathogenic viruses, including Nipah/Hendra, measles and Dengue, indicating that it may represent a common target for therapies for a number of highly virulent/lethal human diseases

High Impact List of Articles
Conference Proceedings

Relevant Topics in Genetics & Molecular Biology

Get the App