IMR Press / FBE / Volume 5 / Issue 1 / DOI: 10.2741/E604

Frontiers in Bioscience-Elite (FBE) is published by IMR Press from Volume 13 Issue 2 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.


How hantaviruses modulate cellular pathways for efficient replication?

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1 Department of Microbiology, Molecular Genetics and Immunology, University of Kansa Medical Center, 3901 Rainbow Boulevard, Kansas City, KS 66103, USA

*Author to whom correspondence should be addressed.


Front. Biosci. (Elite Ed) 2013, 5(1), 154–166;
Published: 1 January 2013

Hantaviruses are zoonotic category-A pathogens that cause highly fatal diseases in humans. The hantaviral genome encodes three viral proteins: RNA-dependent RNA polymerase (RdRp or L protein), nucleocapsid protein (N), and a glycoprotein precursor (GPC), which is posttranslationally cleaved into two surface glycoproteins Gn and Gc. The cytoplasmic tail of Gn interferes with interferon signaling pathways. N is a multifunctional molecule that was shown to be involved in the transcription and translation of viral proteins. N binds to the host mRNA caps and protects the degradation of mRNA 5’ termini, which are later snatched and used as primers by the viral RdRp during transcription initiation. N also seems to lure the host translation machinery for the preferential translation of viral transcripts. Moreover, N was shown to delay the induction of cellular apoptosis and facilitate the transport and localization of viral ribonucleoproteins (RNPs) by exploiting the cellular cytoskeleton and SUMOlyation machinery. Therefore, with their limited protein coding capacity, hantaviruses have evolved several strategies to modulate cellular pathways for their efficient replication.

modulation of cellular pathways by hantaviruses
tail domain
nucleocapsid protein
innate immune response
sumoylation machinery
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