Delpino MV, Quarleri J. Perilipin 2 inhibits replication of hepatitis B virus deoxyribonucleic acid by regulating autophagy under high-fat conditions. World J Virol 2024; 13(1): 90384 [PMID: 38616854 DOI: 10.5501/wjv.v13.i1.90384]
Corresponding Author of This Article
M Victoria Delpino, PhD, Research Scientist, Instituto de Investi-gaciones Biomédicas en Retrovirus y Sida, Universidad de Buenos Aires, Consejo Nacional de Investigaciones Científicas y Técnicas, Paraguay 2155 Piso 11, Buenos Aires 1121, Argentina. mdelpino@ffyb.uba.ar
Research Domain of This Article
Virology
Article-Type of This Article
Editorial
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (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: http://creativecommons.org/licenses/by-nc/4.0/
World J Virol. Mar 25, 2024; 13(1): 90384 Published online Mar 25, 2024. doi: 10.5501/wjv.v13.i1.90384
Perilipin 2 inhibits replication of hepatitis B virus deoxyribonucleic acid by regulating autophagy under high-fat conditions
M Victoria Delpino, Jorge Quarleri
M Victoria Delpino, Jorge Quarleri, Instituto de Investigaciones Biomédicas en Retrovirus y Sida, Universidad de Buenos Aires, Consejo Nacional de Investigaciones Científicas y Técnicas, Buenos Aires 1121, Argentina
Author contributions: Quarleri J and Delpino MV contributed equally to this work. Both authors have read and approved the final manuscript.
Conflict-of-interest statement: All the authors disclose no financial conflicts of interest for this article.
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: M Victoria Delpino, PhD, Research Scientist, Instituto de Investi-gaciones Biomédicas en Retrovirus y Sida, Universidad de Buenos Aires, Consejo Nacional de Investigaciones Científicas y Técnicas, Paraguay 2155 Piso 11, Buenos Aires 1121, Argentina. mdelpino@ffyb.uba.ar
Received: December 1, 2023 Peer-review started: December 1, 2023 First decision: December 7, 2023 Revised: December 7, 2023 Accepted: January 5, 2024 Article in press: January 5, 2024 Published online: March 25, 2024 Processing time: 100 Days and 19.4 Hours
Abstract
Hepatitis B virus (HBV) infection poses a global health concern without a definitive cure; however, antiviral medications can effectively suppress viral replication. This study delves into the intricate interplay between lipid metabolism and HBV replication, implicating molecular mechanisms such as the stearoyl coenzyme A desaturase 1 autophagy pathway, SAC1-like phosphatidylinositol phosphatase, and galectin-9 mediated selective autophagy of viral core proteins in regulating HBV replication. Within lipid droplets, perilipin 2 (PLIN2) emerges as a pivotal guardian, with its overexpression protecting against autophagy and downregulation stimulating triglyceride catabolism through the autophagy pathway. This editorial discusses the correlation between hepatic steatosis and HBV replication, emphasizing the role of PLIN2 in this process. The study underscores the multifaceted roles of lipid metabolism, autophagy, and perilipins in HBV replication, shedding light on potential therapeutic avenues.
Core Tip: Hepatitis B virus (HBV) infection poses a global health concern without a definitive cure. This study delves into the complex interplay between lipid metabolism and HBV replication. It reveals that heightened lipid metabolism may exert an inhibitory effect on HBV replication. Specifically, increased fatty acids lead to the accumulation of lipid droplets and the upregulation of perilipin 2 in hepatocytes. This, in turn, inhibits autophagy and subsequently hinders HBV replication.
