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Dev Comp Immunol. 2016 Apr;57:48-56. doi: 10.1016/j.dci.2015.12.016. Epub 2015 Dec 21.

Zebrafish Plzf transcription factors enhance early type I IFN response induced by two non-enveloped RNA viruses.

Author information

1
INRA, Virologie et Immunologie Moléculaires, 78352 Jouy-en-Josas, France.
2
Institut Pasteur, Unité Macrophages et Développement de l'Immunité, 25-28 rue du Docteur Roux, F-75015 Paris, France; CNRS, URA 2578, F-75015 Paris, France.
3
INRA, Virologie et Immunologie Moléculaires, 78352 Jouy-en-Josas, France. Electronic address: Pierre.Boudinot@jouy.inra.fr.

Abstract

The BTB-POZ transcription factor Promyelocytic Leukemia Zinc Finger (PLZF, or ZBTB16) has been recently identified as a major factor regulating the induction of a subset of Interferon stimulated genes in human and mouse. We show that the two co-orthologues of PLZF found in zebrafish show distinct expression patterns, especially in larvae. Although zbtb16a/plzfa and zbtb16b/plzfb are not modulated by IFN produced during viral infection, their over-expression increases the level of the early type I IFN response, at a critical phase in the race between the virus and the host response. The effect of Plzfb on IFN induction was also detectable after cell infection by different non-enveloped RNA viruses, but not after infection by the rhabdovirus SVCV. Our findings indicate that plzf implication in the regulation of type I IFN responses is conserved across vertebrates, but at multiple levels of the pathway and through different mechanisms.

KEYWORDS:

Antiviral innate immunity; Interferon; PLZF; ZBTB; Zebrafish

PMID:
26719025
DOI:
10.1016/j.dci.2015.12.016
[Indexed for MEDLINE]

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