Partial dysfunction of STAT1 profoundly reduces host resistance to flaviviral infection
| Autor: | Maximilian Larena, Mario Lobigs |
|---|---|
| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
Amino Acid Motifs Locus (genetics) Virus 03 medical and health sciences Mice Interferon Virology medicine Animals Humans STAT1 Gene Genetics biology Flaviviridae Flaviviridae Infections biology.organism_classification Phenotype Mice Inbred C57BL Flavivirus 030104 developmental biology STAT1 Transcription Factor Amino Acid Substitution Knockout mouse Interferon Type I biology.protein medicine.drug |
| Zdroj: | Virology. 506 |
| ISSN: | 1096-0341 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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