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

• Published in: Virus research 2012-10, Vol.169 (1), p.264-267
• Main Authors: Xu, Dequan, Lillico, Simon G., Barnett, Mark W., Whitelaw, Christopher B.A., Archibald, Alan L., Ait-Ali, Tahar
• Format: Article
• Language: English
• 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
• ISSN: 0168-1702; 1872-7492
• DOI: 10.1016/j.virusres.2012.07.002

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.