A role for glycolipid biosynthesis in severe fever with thrombocytopenia syndrome virus entry

• DOI: 10.1371/journal.ppat.1006316
• Publication Date: 2017-04-07T14:14:46Z
• Authors: Mary Jane Drake; Benjamin Brennan; Kenneth Briley Jr; Stephen M. Bart; Eric Sherman; Agnieszka M. Szemiel; Madeleine Minutillo; Frederic D. Bushman; Paul Bates
• Keywords: Phlebovirus

A novel bunyavirus was recently found to cause severe febrile illness with high mortality in agricultural regions of China, Japan, and South Korea. This virus, named fever thrombocytopenia syndrome virus (SFTSV), represents a new group within the Phlebovirus genus Bunyaviridae. Little is known about viral entry requirements beyond showing dependence on dynamin endosomal acidification. haploid forward genetic screen performed identify host cell for SFTSV entry. The identified glucosylceramide synthase (ugcg), enzyme responsible initiating de novo glycosphingolipid biosynthesis. Genetic pharmacological approaches confirmed that UGCG expression enzymatic activity were required efficient Furthermore, inhibition affected post-internalization stage entry, leading accumulation particles enlarged cytoplasmic structures, suggesting impaired trafficking and/or fusion membranes. These findings specify role provide target antiviral therapies.