Expression of interferon-induced antiviral genes is delayed in a STAT1 knockout mouse model of Crimean-Congo hemorrhagic fever

Virology Journal

Dennis A Bente²  Adriana M Airo³  Gavin C Bowick¹ 

[1] Center for Tropical Diseases, University of Texas Medical Branch, Galveston, TX, USA;Department of Microbiology & Immunology, 301 University Boulevard, Galveston, TX, 77555-0610, USA;Special Pathogens Program, National Microbiology Laboratory, Public Health Agency of Canada, Winnipeg, MB, Canada

关键词: STAT1;    Signaling;    Animal model;    Interferon;    Crimean Congo hemorrhagic fever;   

Others  :  1154441
DOI  :  10.1186/1743-422X-9-122

 received in 2011-11-23, accepted in 2012-06-19,  发布年份 2012

【 摘 要 】

Background

Crimean Congo hemorrhagic fever (CCHF) is a tick-borne hemorrhagic zoonosis associated with high mortality. Pathogenesis studies and the development of vaccines and antivirals against CCHF have been severely hampered by the lack of suitable animal model. We recently developed and characterized a mature mouse model for CCHF using mice carrying STAT1 knockout (KO).

Findings

Given the importance of interferons in controlling viral infections, we investigated the expression of interferon pathway-associated genes in KO and wild-type (WT) mice challenged with CCHF virus. We expected that the absence of the STAT1 protein would result in minimal expression of IFN-related genes. Surprisingly, the KO mice showed high levels of IFN-stimulated gene expression, beginning on day 2 post-infection, while in WT mice challenged with virus the same genes were expressed at similar levels on day 1.

Conclusions

We conclude that CCHF virus induces similar type I IFN responses in STAT1 KO and WT mice, but the delayed response in the KO mice permits rapid viral dissemination and fatal illness.

【 授权许可】

   
2012 Bowick et al.; licensee BioMed Central Ltd.

【 图 表 】

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