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Chicken CH25H inhibits ALV-J replication by promoting cellular autophagy

Autophagy plays an important role in host antiviral defense. The avian leukosis virus subgroup J (ALV-J) has been shown to inhibit autophagy while promoting viral replication. The underlying autophagic mechanisms, however, are unknown. Cholesterol 25-hydroxylase (CH25H) is a conserved interferon-sti...

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Autores principales: Xie, Tingting, Feng, Min, Zhang, Xi, Li, Xiaoqi, Mo, Guodong, Shi, Meiqing, Zhang, Xiquan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9975585/
https://www.ncbi.nlm.nih.gov/pubmed/36875122
http://dx.doi.org/10.3389/fimmu.2023.1093289
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author Xie, Tingting
Feng, Min
Zhang, Xi
Li, Xiaoqi
Mo, Guodong
Shi, Meiqing
Zhang, Xiquan
author_facet Xie, Tingting
Feng, Min
Zhang, Xi
Li, Xiaoqi
Mo, Guodong
Shi, Meiqing
Zhang, Xiquan
author_sort Xie, Tingting
collection PubMed
description Autophagy plays an important role in host antiviral defense. The avian leukosis virus subgroup J (ALV-J) has been shown to inhibit autophagy while promoting viral replication. The underlying autophagic mechanisms, however, are unknown. Cholesterol 25-hydroxylase (CH25H) is a conserved interferon-stimulated gene, which converts cholesterol to a soluble antiviral factor, 25-hydroxycholesterol (25HC). In this study, we further investigated the autophagic mechanism of CH25H resistance to ALV-J in chicken embryonic fibroblast cell lines (DF1). Our results found that overexpression of CH25H and treatment with 25HC promoted the autophagic markers microtubule-associated protein 1 light chain 3 II (LC3II) and autophagy-related gene 5(ATG5), while decreased autophagy substrate p62/SQSTM1 (p62) expression in ALV-J infection DF-1 cells. Induction of cellular autophagy also reduces the levels of ALV-J gp85 and p27. ALV-J infection, on the other hand, suppresses autophagic marker protein LC3II expression. These findings suggest that CH25H-induced autophagy is a host defense mechanism that aids in ALV-J replication inhibition. In particular, CH25H interacts with CHMP4B and inhibits ALV-J infection in DF-1 cells by promoting autophagy, revealing a novel mechanism by which CH25H inhibits ALV-J infection. Although the underlying mechanisms are not completely understood, CH25H and 25HC are the first to show inhibiting ALV-J infection via autophagy.
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spelling pubmed-99755852023-03-02 Chicken CH25H inhibits ALV-J replication by promoting cellular autophagy Xie, Tingting Feng, Min Zhang, Xi Li, Xiaoqi Mo, Guodong Shi, Meiqing Zhang, Xiquan Front Immunol Immunology Autophagy plays an important role in host antiviral defense. The avian leukosis virus subgroup J (ALV-J) has been shown to inhibit autophagy while promoting viral replication. The underlying autophagic mechanisms, however, are unknown. Cholesterol 25-hydroxylase (CH25H) is a conserved interferon-stimulated gene, which converts cholesterol to a soluble antiviral factor, 25-hydroxycholesterol (25HC). In this study, we further investigated the autophagic mechanism of CH25H resistance to ALV-J in chicken embryonic fibroblast cell lines (DF1). Our results found that overexpression of CH25H and treatment with 25HC promoted the autophagic markers microtubule-associated protein 1 light chain 3 II (LC3II) and autophagy-related gene 5(ATG5), while decreased autophagy substrate p62/SQSTM1 (p62) expression in ALV-J infection DF-1 cells. Induction of cellular autophagy also reduces the levels of ALV-J gp85 and p27. ALV-J infection, on the other hand, suppresses autophagic marker protein LC3II expression. These findings suggest that CH25H-induced autophagy is a host defense mechanism that aids in ALV-J replication inhibition. In particular, CH25H interacts with CHMP4B and inhibits ALV-J infection in DF-1 cells by promoting autophagy, revealing a novel mechanism by which CH25H inhibits ALV-J infection. Although the underlying mechanisms are not completely understood, CH25H and 25HC are the first to show inhibiting ALV-J infection via autophagy. Frontiers Media S.A. 2023-02-15 /pmc/articles/PMC9975585/ /pubmed/36875122 http://dx.doi.org/10.3389/fimmu.2023.1093289 Text en Copyright © 2023 Xie, Feng, Zhang, Li, Mo, Shi and Zhang https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Immunology
Xie, Tingting
Feng, Min
Zhang, Xi
Li, Xiaoqi
Mo, Guodong
Shi, Meiqing
Zhang, Xiquan
Chicken CH25H inhibits ALV-J replication by promoting cellular autophagy
title Chicken CH25H inhibits ALV-J replication by promoting cellular autophagy
title_full Chicken CH25H inhibits ALV-J replication by promoting cellular autophagy
title_fullStr Chicken CH25H inhibits ALV-J replication by promoting cellular autophagy
title_full_unstemmed Chicken CH25H inhibits ALV-J replication by promoting cellular autophagy
title_short Chicken CH25H inhibits ALV-J replication by promoting cellular autophagy
title_sort chicken ch25h inhibits alv-j replication by promoting cellular autophagy
topic Immunology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9975585/
https://www.ncbi.nlm.nih.gov/pubmed/36875122
http://dx.doi.org/10.3389/fimmu.2023.1093289
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