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

Kelsey A Haugh, Natalia Shalginskikh, Shoko Nogusa, Anna Marie Skalka, Richard A Katz* and Siddharth Balachandran*

Author Affiliations

Immune Cell Development and Host Defense Program, Fox Chase Cancer Center, Room 422 Reimann Building, 333 Cottman Ave., 19111 Philadelphia, PA, USA

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Virology Journal 2014, 11:100  doi:10.1186/1743-422X-11-100

Published: 28 May 2014



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 (α/β) 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.


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.


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.

Daxx; Interferon; Avian sarcoma virus; Innate immunity