Basic Study
Copyright ©The Author(s) 2023. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Virol. Dec 25, 2023; 12(5): 296-308
Published online Dec 25, 2023. doi: 10.5501/wjv.v12.i5.296
Perilipin2 inhibits the replication of hepatitis B virus deoxyribonucleic acid by regulating autophagy under high-fat conditions
Chuang Wang, Xiao-Yun Gao, Mei Han, Meng-Chun Jiang, Xiao-Yi Shi, Chun-Wen Pu, Xuan Du
Chuang Wang, Xiao-Yi Shi, Graduate School, Graduate School of Dalian Medical University, Dalian 116000, Liaoning Province, China
Xiao-Yun Gao, Department of Geriatric, The Second Affiliated Hospital of Dalian Medical University, Dalian 116023, Liaoning Province, China
Mei Han, Meng-Chun Jiang, Xuan Du, Department of Gastroenterology, The Second Affiliated Hospital of Dalian Medical University, Dalian 116023, Liaoning Province, China
Chun-Wen Pu, Dalian Public Health Clinical Center, Dalian Municipal Research Institute for Public Health, Dalian 116001, Liaoning Province, China
Co-first authors: Chuang Wang and Xiao-Yun Gao.
Co-corresponding authors: Chun-Wen Pu and Xuan Du.
Author contributions: Du X and Gao XY designed the experiment and drafted the manuscript; Wang C performed the experiments; Du X and Wang C participated in the statistical analyses; Han M, Shi XY, and Jiang CM helped draft the manuscript; All authors have read and approved the final manuscript.
Institutional review board statement: The study has been approved by the Ethics Committee of Dalian Sixth People's Hospital. The privacy rights of human subjects were always respected during human experimentation, and informed consent was obtained prior to the experiment. The ethics program number is DLY/CB-IRB-026.
Institutional animal care and use committee statement: This study does not involve animal experiments.
Informed consent statement: All study participants or their legal guardian provided informed written consent about personal and medical data collection prior to study enrolment.
Conflict-of-interest statement: All the authors declare that they have no conflict of interest.
Data sharing statement: No additional data are available.
ARRIVE guidelines statement: The authors have read the ARRIVE guidelines, and the manuscript was prepared and revised according to the ARRIVE guidelines.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Xuan Du, PhD, Doctor, Department of Gastroenterology, The Second Affiliated Hospital of Dalian Medical University, No. 467 Zhongshan Road, Shahekou District, Dalian 116023, Liaoning Province, China. duxuan945@163.com
Received: September 11, 2023
Peer-review started: September 11, 2023
First decision: October 9, 2023
Revised: October 19, 2023
Accepted: November 30, 2023
Article in press: November 30, 2023
Published online: December 25, 2023
ARTICLE HIGHLIGHTS
Research background

The relationship between lipid metabolism and hepatitis B virus (HBV) deoxyribonucleic acid (DNA) replication and its underlying mechanisms are not well understood.

Research motivation

To investigate the relationship between lipid metabolism and HBV DNA replication and its underlying mechanisms.

Research objectives

We speculated that the Plin2-autophagy pathway might be involved in regulating lipid deposition and HBV replication in hepatocytes.

Research methods

We first explored the relationship between patients' lipid levels and HBV DNA load. Also, we constructed an HBV infection combined with a hepatic steatosis cell model in vitro.

Research results

Stratified analysis by HBeAg showed significant negative correlations between HBV-DNA load and hepatic steatosis ratio in both HBeAg-positive group and in HBeAg-negative group. The results of in vitro experiments suggested that fatty acid treatment increased the lipid droplets deposition and decreased the cell supernatant HBsAg, HBeAg expression and HBV DNA load.

Research conclusions

Fatty acid stimulation inhibits HBV replication by upregulating Plin2 expression, inhibiting hepatocyte autophagy.

Research perspectives

A possible route for treating patients with chronic HBV infection combined with nonalcoholic fatty liver disease.