USP18 restricts PRRSV growth through alteration of nuclear translocation of NF-κB p65 and p50 in MARC-145 cells

Although the functions of porcine respiratory and reproductive syndrome virus (PRRSV) proteins are increasingly understood, the roles of host factors in modifying infection are less well understood. Growing evidence places deubiquitination at the core of a multitude of regulatory processes, ranging...

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Bibliographic Details
Published in:	Virus research Vol. 169; no. 1; pp. 264 - 267
Main Authors:	Xu, Dequan, Lillico, Simon G., Barnett, Mark W., Whitelaw, Christopher B.A., Archibald, Alan L., Ait-Ali, Tahar
Format:	Journal Article
Language:	English
Published:	Netherlands Elsevier B.V 01-10-2012 Elsevier Science
Subjects:	Animals cell growth Cell Line Endopeptidases - metabolism Haplorhini Immunity, Innate infectious diseases innate immunity MARC-145 microbial growth NF-kappa B p50 Subunit - metabolism NF-κB Pig Porcine reproductive and respiratory syndrome virus Porcine respiratory and reproductive syndrome virus Porcine respiratory and reproductive syndrome virus - growth & development Porcine respiratory and reproductive syndrome virus - immunology Protein Transport proteins PRRSV Short Communication swine transcription factor NF-kappa B Transcription Factor RelA - metabolism Ubiquitins - metabolism USP18 MARC-145 NF-κB USP18 PRRSV Pig
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Summary:	Although the functions of porcine respiratory and reproductive syndrome virus (PRRSV) proteins are increasingly understood, the roles of host factors in modifying infection are less well understood. Growing evidence places deubiquitination at the core of a multitude of regulatory processes, ranging from cell growth to innate immune response and health, such as cancer, degenerative and infectious diseases. This report provides further information on the functional role of the porcine ubiquitin-specific peptidase 18 (USP18) during innate immune responses to PRRSV. We have shown that constitutive overexpression of the porcine USP18 in MARC-145 cells restricts PRRSV growth, at least in part via early activation of NF-κB. Viral growth of PRRSV may be perturbed by increasing and decreasing nuclear translocation of p65 and p50, respectively. Our data highlight USP18 as a host restriction factor during innate immune response to PRRSV.
Bibliography:	http://dx.doi.org/10.1016/j.virusres.2012.07.002 ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 ObjectType-Article-2 ObjectType-Feature-1
ISSN:	0168-1702 1872-7492
DOI:	10.1016/j.virusres.2012.07.002