Journal ArticleDOI
The Carboxyl-Half of the Rotavirus Nonstructural Protein NS53 (NSP1) Is Not Required for Virus Replication
Jian Hua,John T. Patton +1 more
TLDR
Results demonstrate that the carboxyl-terminal 233 aa of NS53 are not required for rotavirus replication in vitro, and provide evidence that the subcellular localization signal in NS53 resides in the amino terminal half of the protein.About:
This article is published in Virology.The article was published on 1994-02-01. It has received 65 citations till now. The article focuses on the topics: NSP1 & Gene rearrangement.read more
Citations
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Journal ArticleDOI
Rotavirus Replication: Plus-Sense Templates for Double-Stranded RNA Synthesis Are Made in Viroplasms
TL;DR: It is proposed that plus-strand RNAs synthesized within viroplasms are the primary source of templates for genome replication and that trafficking pathways do not exist within the cytosol that transport plus-strate RNAs to viroPLasms.
Journal ArticleDOI
Entirely plasmid-based reverse genetics system for rotaviruses
Yuta Kanai,Satoshi Komoto,Takahiro Kawagishi,Ryotaro Nouda,Naoko Nagasawa,Misa Onishi,Yoshiharu Matsuura,Koki Taniguchi,Takeshi Kobayashi +8 more
TL;DR: A plasmid-based reverse genetics system that is free from helper viruses and independent of any selection for RV is developed, which will accelerate studies of RV pathobiology, allow rational design of RV vaccines, and yield RVs suitable for screening small molecules as potential antivirals.
Journal ArticleDOI
Genetics of the rotaviruses
TL;DR: Development of a reverse genetic system will facilitate analysis of the molecular mechanisms involved in various genetic, biochemical, and biological phenomena of the rotavirus.
Book ChapterDOI
Genome Rearrangements of Rotaviruses
TL;DR: Evidence of rearranged genomes in rotaviruses is described and possible mechanisms of their emergence are discussed, and the significance of genome rearrangements for viral evolution is considered.
Journal ArticleDOI
Interferon Regulatory Factor 3 Is a Cellular Partner of Rotavirus NSP1
TL;DR: It is predicted that a role for NSP1 in rotavirus-infected cells is to inhibit activation of IRF-3 and diminish the cellular interferon response.