The regulation of persistent Borna disease virus infection by RNA silencing factors in human cells.

Autor: Kaneko Y; Department of Biochemistry and Molecular Biology, Graduate School of Science and Engineering, Saitama University, Saitama, 338-8570, Japan., Naito Y; Department of Biochemistry and Molecular Biology, Faculty of Science, Saitama University, Saitama, 338-8570, Japan., Koide R; Genome Immunobiology RIKEN Hakubi Research Team, Cluster for Pioneering Research, RIKEN, Yokohama, 235-0045, Japan; Center for Integrative Medical Sciences, RIKEN, Yokohama, 235-0045, Japan., Parrish NF; Genome Immunobiology RIKEN Hakubi Research Team, Cluster for Pioneering Research, RIKEN, Yokohama, 235-0045, Japan; Center for Integrative Medical Sciences, RIKEN, Yokohama, 235-0045, Japan., Takahashi T; Department of Biochemistry and Molecular Biology, Graduate School of Science and Engineering, Saitama University, Saitama, 338-8570, Japan. Electronic address: takahas@mail.saitama-u.ac.jp.
Jazyk: angličtina
Zdroj: Biochemical and biophysical research communications [Biochem Biophys Res Commun] 2023 May 28; Vol. 658, pp. 122-127. Date of Electronic Publication: 2023 Mar 31.
DOI: 10.1016/j.bbrc.2023.03.069
Abstrakt: Viral infection induces diverse cellular immune responses. Some viruses induce the production of antiviral cytokines, alterations of endogenous gene expression, and apoptosis; however, other viruses replicate without inducing such responses, enabling them to persistently infect cells. Infection by Borna disease virus type 1 (BoDV-1) can result in fatal immune-mediated encephalitis, including in humans, yet infection of cells in vitro is generally persistent. The regulatory mechanisms underlying this persistent infection remain unclear. Here, we show that an enhancer of RNA-silencing, TRBP, positively regulates BoDV RNA level in human cells. Knockdown of TRBP decreased BoDV RNA levels in persistently-infected cells, whereas overexpression of TRBP increased BoDV RNA levels. To investigate the mechanism underlying this phenomenon, we performed immunoprecipitation assays and found that TRBP interacts with BoDV RNA. Furthermore, we performed cell fractionation, which revealed that persistent infection with BoDV does not alter the localization of TRBP and other RNA silencing factors in cells. Our results showed the regulation of persistent BoDV infection by RNA-silencing factors in human cells.
Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2023 Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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