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Published on: December 29, 2015
Bunyavirus N: eIF4F surrogate and cap-guardian
Antonito T Panganiban1, Mohammad A Mir
1Department of Molecular Genetics and Microbiology and Center for Infectious Diseases and Immunity, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA. apanganiban@salud.unm.edu
Abstract:
Hantaviruses comprise a genus of the bunyavirus family of viruses. Viruses of this family, along with the arenaviruses, and the orthomyxoviruses, including influenza, contain a negative sense, segmented RNA genome. Viral nucleocapsid proteins play a well-established role in the formation of intracellular and virion-associated nucleocapsids that harbor and shield viral genomic RNA. However, recent observations indicate that hantavirus nucleocapsid protein (N) has additional unexpected biological activities that interface with both the cellular mRNA translation and mRNA degradation apparatus. N has an activity that mimics or circumvents the cellular cap-binding complex, eIF4F, in the initial stages of translation initiation. As a consequence of its translation initiation activity, N can augment translational expression. In addition to its ability to enhance translation initiation, N co-localizes with the cellular peptides that mediate mRNA decay. mRNA decay often takes place in cytoplasmic processing bodies (P-bodies), and N is abundant in P bodies. The association of N with P bodies enables cap-snatching for viral transcription initiation. It is likely that these two surprising new activities of N function in concert during bunyavirus gene expression. All these activities of N revolve around the ability of N to recognize RNA in a correct, context-dependent manner.
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