Bub1 Facilitates Virus Entry through Endocytosis in a Model of Drosophila Pathogenesis.

ABSTRACT: In order to establish productive infection and dissemination, viruses usually evolve a number of strategies to hijack and/or subvert the host defense systems. However, host factors utilized by the virus to facilitate infection remain poorly characterized. In this work, we found that Drosophila melanogaster deficient in budding uninhibited by benzimidazoles 1 (bub1), a highly conserved subunit of the kinetochore complex regulating chromosome congression (1), became resistant to Drosophila C virus (DCV) infection, evidenced in increased survival rates and reduced viral loads, compared to the wild-type control. Mechanistic analysis further showed that Bub1 also functioned in the cytoplasm and was essentially involved in clathrin-dependent endocytosis of DCV and oth

SUBMITTER: Yang S 

PROVIDER: S-EPMC6146689 | biostudies-literature | 2018 Sep

REPOSITORIES: biostudies-literature