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Fatty acid translocase promoted hepatitis B virus replication by upregulating the levels of hepatic cytosolic calcium

Huang, J; Zhao, L; Yang, P; Chen, Z; Ruan, XZ; Huang, A; Tang, N; (2017) Fatty acid translocase promoted hepatitis B virus replication by upregulating the levels of hepatic cytosolic calcium. Experimental Cell Research , 358 (2) pp. 360-368. 10.1016/j.yexcr.2017.07.012. Green open access

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Abstract

Hepatitis B virus (HBV) is designated a “metabolovirus” due to the intimate connection between the virus and host metabolism. The nutrition state of the host plays a relevant role in the severity of HBV infection. Metabolic syndrome (MS) is prone to increasing HBV DNA loads and accelerating the progression of liver disease in patients with chronic hepatitis B (CHB). Cluster of differentiation 36 (CD36), also named fatty acid translocase, is known to facilitate long-chain fatty acid uptake and contribute to the development of MS. We recently found that CD36 overexpression enhanced HBV replication. In this study, we further explored the mechanism by which CD36 overexpression promotes HBV replication. Our data showed that CD36 overexpression increased HBV replication, and CD36 knockdown inhibited HBV replication. RNA sequencing found some of the differentially expressed genes were involved in calcium ion homeostasis. CD36 overexpression elevated the cytosolic calcium level, and CD36 knockdown decreased the cytosolic calcium level. Calcium chelator BAPTA-AM could override the HBV replication increased by CD36 overexpression, and the calcium activator thapsigargin could improve the HBV replication reduced by CD36 knockdown. We further found that CD36 overexpression activated Src kinase, which plays an important role in the regulation of the store-operated Ca2+ channel. An inhibitor of Src kinase (SU6656) significantly reduced the CD36-induced HBV replication. We identified a novel link between CD36 and HBV replication, which is associated with cytosolic calcium and the Src kinase pathway. CD36 may represent a potential therapeutic target for the treatment of CHB patients with MS.

Type: Article
Title: Fatty acid translocase promoted hepatitis B virus replication by upregulating the levels of hepatic cytosolic calcium
Open access status: An open access version is available from UCL Discovery
DOI: 10.1016/j.yexcr.2017.07.012
Publisher version: https://doi.org/10.1016/j.yexcr.2017.07.012
Language: English
Additional information: This version is the author accepted manuscript. For information on re-use, please refer to the publisher’s terms and conditions.
Keywords: Science & Technology, Life Sciences & Biomedicine, Oncology, Cell Biology, CD36, Hepatitis B Virus, Replication, Cytosolic Calcium, Src Kinase, Transgenic Mice, Surface-Antigen, Metabolic Syndrome, Viral-Proteins, Mouse Model, Cells, Expression, Infection, Signals
UCL classification: UCL
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Medical Sciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Medical Sciences > Div of Medicine
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Medical Sciences > Div of Medicine > Renal Medicine
URI: https://discovery.ucl.ac.uk/id/eprint/10050716
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