MicroRNA antagonism of the picornaviral life cycle: alternative mechanisms of interference.
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In addition to modulating the function and stability of cellular mRNAs, microRNAs can profoundly affect the life cycles of viruses bearing sequence complementary targets, a finding recently exploited to ameliorate toxicities of vaccines and oncolytic viruses. To elucidate the mechanisms underlying microRNA-mediated antiviral activity, we modified the 3' untranslated region (3'UTR) of Coxsackievirus A21 to incorporate targets with varying degrees of homology to endogenous microRNAs. We show that microRNAs can interrupt the picornavirus life-cycle at multiple levels, including catalytic degradation of the viral RNA genome, suppression of cap-independent mRNA translation, and interference with genome encapsidation. In addition, we have examined the extent to which endogenous microRNAs can suppress viral replication in vivo and how viruses can overcome this inhibition by microRNA saturation in mouse cancer models.
Subject3' Untranslated Regions
Disease Models, Animal
Leukemia, Lymphocytic, Chronic, B-Cell
Molecular Sequence Data
Published Version (Please cite this version)10.1371/journal.ppat.1000820
Publication InfoKelly, Elizabeth J; Hadac, Elizabeth M; Cullen, Bryan R; & Russell, Stephen J (2010). MicroRNA antagonism of the picornaviral life cycle: alternative mechanisms of interference. PLoS Pathog, 6(3). pp. e1000820. 10.1371/journal.ppat.1000820. Retrieved from https://hdl.handle.net/10161/4597.
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James B. Duke Distinguished Professor of Molecular Genetics and Microbiology
My laboratory has for sometime been interested in understanding the molecular biology of the replication cycle of the pathogenic retrovirus HIV-1. Because HIV-1 gene expression is primarily regulated by specific RNA:protein interactions, my laboratory has also become interested in the more general area of RNA sequence mediated gene regulation, including nuclear mRNA export and the phenomenon of RNA interference. In the past, my laboratory has worked extensively on Tat, the trans