The interferon-inducible antiviral protein Daxx is not essential for interferon-mediated protection against avian sarcoma virus

被引:6
|
作者
Haugh, Kelsey A. [1 ]
Shalginskikh, Natalia [1 ]
Nogusa, Shoko [1 ]
Skalka, Anna Marie [1 ]
Katz, Richard A. [1 ]
Balachandran, Siddharth [1 ]
机构
[1] Fox Chase Canc Ctr, Immune Cell Dev & Host Def Program, Philadelphia, PA 19111 USA
来源
VIROLOGY JOURNAL | 2014年 / 11卷
基金
美国国家卫生研究院;
关键词
Daxx; Interferon; Avian sarcoma virus; Innate immunity; VESICULAR STOMATITIS-VIRUS; IMMUNITY; VECTORS; CELLS; DNA;
D O I
10.1186/1743-422X-11-100
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Background: The antiviral protein Daxx acts as a restriction factor of avian sarcoma virus (ASV; Retroviridae) in mammalian cells by promoting epigenetic silencing of integrated proviral DNA. Although Daxx is encoded by a type I (alpha/beta) interferon-stimulated gene, the requirement for Daxx in the interferon anti-retroviral response has not been elucidated. In this report, we describe the results of experiments designed to investigate the role of Daxx in the type I interferon-induced anti-ASV response. Findings: Using an ASV reporter system, we show that type I interferons are potent inhibitors of ASV replication. We demonstrate that, while Daxx is necessary to silence ASV gene expression in the absence of interferons, type I interferons are fully-capable of inducing an antiviral state in the absence of Daxx. Conclusions: These results provide evidence that Daxx is not essential for the anti-ASV interferon response in mammalian cells, and that interferons deploy multiple, redundant antiviral mechanisms to protect cells from ASV.
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页数:5
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