| Literature DB >> 31801065 |
Anastasia Hyrina1, Christopher Jones2, Darlene Chen2, Scott Clarkson3, Nadire Cochran3, Paul Feucht2, Gregory Hoffman3, Alicia Lindeman3, Carsten Russ3, Frederic Sigoillot3, Tiffany Tsang2, Kyoko Uehara2, Lili Xie2, Don Ganem2, Meghan Holdorf2.
Abstract
A hallmark of chronic hepatitis B (CHB) virus infection is the presence of high circulating levels of non-infectious small lipid HBV surface antigen (HBsAg) vesicles. Although rare, sustained HBsAg loss is the idealized endpoint of any CHB therapy. A small molecule, RG7834, has been previously reported to inhibit HBsAg expression by targeting terminal nucleotidyltransferase proteins 4A and 4B (TENT4A and TENT4B). In this study, we describe a genome-wide CRISPR screen to identify other potential host factors required for HBsAg expression and to gain further insights into the mechanism of RG7834. We report more than 60 genes involved in regulating HBsAg and identify additional factors involved in RG7834 activity, including a zinc finger CCHC-type containing 14 (ZCCHC14) protein. We show that ZCCHC14, together with TENT4A/B, stabilizes HBsAg expression through HBV RNA tailing, providing a potential new therapeutic target to achieve functional cure in CHB patients.Entities:
Keywords: CRISPR; HBV; HBsAg; RG7834; RNA tailing; TENT4B; ZCCHC14; genome-wide screen
Year: 2019 PMID: 31801065 DOI: 10.1016/j.celrep.2019.10.113
Source DB: PubMed Journal: Cell Rep Impact factor: 9.423