Disruption of clathrin-dependent trafficking results in the failure of grass carp reovirus cellular entry. Issue 1 (December 2016)

• Record Type: Journal Article
• Authors: Wang, Hao; Liu, Weisha; Yu, Fei; Lu, Liqun
• Is Part Of: Virology journal. Volume 13:Issue 1(2016)
• Page Start: 1
• Page End: 10
• Publication Date: 2016-12
• Subjects: Ctenopharyngodon idellus -- Clathrin -- GCRV -- Ammonium chloride -- Viral entry; Virology -- Periodicals; 579.2
• DOI: 10.1186/s12985-016-0485-7
• Languages: English
• ISSNs: 1743-422X

Abstract

Abstract Background Grass carp reovirus (GCRV) is responsible for viral hemorrhagic disease in cultured grass carp (Ctenopharyngon idellus ). GCRV is a non-enveloped, double-stranded RNA virus in the genusAquareovirus, of the familyReoviridae, which encodes seven structural proteins (VP1-VP7) and five nonstructural proteins (NS80, NS38, NS31, NS26, and NS16). To date, the mechanism of GCRV entry into CIKCtenopharyngon idellus kidney (CIK) cells remains poorly understood. Results Here, we present a study of the GCRV internalization mechanism in CIK cells. Our results indicated that GCRV infection was inhibited by chlorpromazine, the specific inhibitor for clathrin-mediated endocytosis. Colocalization of GCRV virions with endogenous clathrin was observed during early infection by confocal microscopy. Moreover, GCRV infection of CIK cells depended on acidification of the endosome. This was indicated by significant inhibition of viral infection following prophylactic treatment with the lysosomotropic drugs chloroquine or ammonium chloride. In addition, the disturbance of dynamin activity blocked GCRV entry, which confirmed the dynamin-dependent nature of clathrin-mediated endocytosis. Conclusion Our findings suggest that GCRV might enter CIK cells via clathrin-mediated endocytosis in a pH-dependent manner. Additionally, dynamin is critical for efficient viral entry.