Proteases of Human rhinovirus

Role in infection

Erin WALKER, David Jans, Reena GHILDYAL

Research output: A Conference proceeding or a Chapter in BookChapter

12 Citations (Scopus)

Abstract

Human rhinoviruses (HRV) are the major etiological agents of the common cold and asthma exacerbations, with significant worldwide health and economic impact. Although large-scale population vaccination has proved successful in limiting or even eradicating many viruses, the more than 100 distinct serotypes mean that conventional vaccination is not a feasible strategy to combat HRV. An alternative strategy is to target conserved viral proteins such as the HRV proteases, 2A pro and 3C pro, the focus of this review. Necessary for host cell shutoff, virus replication, and pathogenesis, 2A pro and 3C pro are clearly viable drug targets, and indeed, 3C pro has been successfully targeted for treating the common cold in experimental infection. 2A pro and 3C pro are crucial for virus replication due to their role in polyprotein processing as well as cleavage of key cellular proteins to inhibit cellular transcription and translation. Intriguingly, the action of the HRV proteases also disrupts nucleocytoplasmic trafficking, contributing to HRV cytopathic effects. Improved understanding of the protease-cell interactions should enable new therapeutic approaches to be identified for drug development.

Original languageEnglish
Title of host publicationRhinoviruses
Subtitle of host publicationMethods and Protocols
EditorsD.A Jans, R Ghildyal
Place of PublicationUSA
PublisherHumana Press
Pages129-141
Number of pages13
Volume1221
ISBN (Print)9781493915705
DOIs
Publication statusPublished - 2015

Publication series

NameMethods in Molecular Biology
ISSN (Print)1064-3745

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WALKER, E., Jans, D., & GHILDYAL, R. (2015). Proteases of Human rhinovirus: Role in infection. In D. A. Jans, & R. Ghildyal (Eds.), Rhinoviruses: Methods and Protocols (Vol. 1221, pp. 129-141). (Methods in Molecular Biology). USA: Humana Press. https://doi.org/10.1007/978-1-4939-1571-2_10