Partial dysfunction of STAT1 profoundly reduces host resistance to flaviviral infection

Larena, Maximilian and Lobigs, Mario (2017) Partial dysfunction of STAT1 profoundly reduces host resistance to flaviviral infection. Virology, 506 1-6. doi:10.1016/j.virol.2017.03.001


Author Larena, Maximilian
Lobigs, Mario
Title Partial dysfunction of STAT1 profoundly reduces host resistance to flaviviral infection
Journal name Virology   Check publisher's open access policy
ISSN 1096-0341
0042-6822
Publication date 2017-06-01
Sub-type Article (original research)
DOI 10.1016/j.virol.2017.03.001
Open Access Status Not yet assessed
Volume 506
Start page 1
End page 6
Total pages 6
Place of publication Waltham, MA, United States
Publisher Academic Press
Collection year 2018
Language eng
Formatted abstract
The genetic basis for a dramatically increased virus susceptibility phenotype of MHC-II knockout mice acquired during routine maintenance of the mouse strain was determined. Segregation of the susceptibility allele from the defective MHC-II locus combined with sequence capture and sequencing showed that a Y37L substitution in STAT1 accounted for high flavivirus susceptibility of a newly derived mouse strain, designated Tuara. Interestingly, the mutation in STAT1 gene gave only partial inactivation of the type I interferon antiviral pathway. Accordingly, merely a relatively small impairment of interferon α/β signalling is sufficient to overcome the ability of the host to control the infection.
Keyword Flavivirus
Genetic mapping
Interferon
Japanese encephalitis virus
Spontaneous mutation
STAT1
West nile virus
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: HERDC Pre-Audit
School of Chemistry and Molecular Biosciences
 
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