Peroxisomes are platforms for cytomegalovirus’ evasion from the cellular immune response

• Verfasst von: Magalhães, Ana Cristina [VerfasserIn]
• Verfasst von: Islinger, Markus [VerfasserIn]
• Titel: Peroxisomes are platforms for cytomegalovirus’ evasion from the cellular immune response
• Verf.angabe: Ana Cristina Magalhães, Ana Rita Ferreira, Sílvia Gomes, Marta Vieira, Ana Gouveia, Isabel Valença, Markus Islinger, Rute Nascimento, Michael Schrader, Jonathan C. Kagan and Daniela Ribeiro
• E-Jahr: 2016
• Jahr: 16 May 2016
• Umfang: 14 S.
• Fussnoten: Gesehen am 09.05.2019
• Titel Quelle: Enthalten in: Scientific reports
• Ort Quelle: [London] : Springer Nature, 2011
• Jahr Quelle: 2016
• Band/Heft Quelle: 6(2016) Artikel-Nummer 26028, 14 Seiten
• ISSN Quelle: 2045-2322
• DOI: doi:10.1038/srep26028
• Datenträger: Online-Ressource
• Sprache: eng
• K10plus-PPN: 1665052481

Abstract

The human cytomegalovirus developed distinct evasion mechanisms from the cellular antiviral response involving vMIA, a virally-encoded protein that is not only able to prevent cellular apoptosis but also to inhibit signalling downstream from mitochondrial MAVS. vMIA has been shown to localize at mitochondria and to trigger their fragmentation, a phenomenon proven to be essential for the signalling inhibition. Here, we demonstrate that vMIA is also localized at peroxisomes, induces their fragmentation and inhibits the peroxisomal-dependent antiviral signalling pathway. Importantly, we demonstrate that peroxisomal fragmentation is not essential for vMIA to specifically inhibit signalling downstream the peroxisomal MAVS. We also show that vMIA interacts with the cytoplasmic chaperone Pex19, suggesting that the virus has developed a strategy to highjack the peroxisomal membrane proteins’ transport machinery. Furthermore, we show that vMIA is able to specifically interact with the peroxisomal MAVS. Our results demonstrate that peroxisomes constitute a platform for evasion of the cellular antiviral response and that the human cytomegalovirus has developed a mechanism by which it is able to specifically evade the peroxisomal MAVS-dependent antiviral signalling.