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Peer-reviewedCC BY 4.0Frontiers in Immunology

Advances in endoplasmic reticulum autophagy and its role in viral infection

  • Yulin He1,2
  • Yaxing Su1,2
  • Qing Xu1,2
  • Zhibiao Bian1
  • Pinpin Chu1
  • Chunling Li1
  • Shao-lun Zhai1
  • Yan Li1
  • Zhiyong Jiang1
  • Xia Zhou1
  • Hongchao Gou1
  • Huahua Kang1
  1. 1Institute of Animal Health, Guangdong Academy of Agricultural Sciences, Guangdong Provincial Key Laboratory of Livestock Disease Prevention, Scientific Observation and Experiment Station of Veterinary Drugs and Diagnostic Techniques of Guangdong Province, Guangdong Provincial Key Laboratory of Research on the Technology of Pig-breeding and Pig-disease prevention
  2. 2College of Veterinary Medicine, South China Agricultural University, Guangdong Laboratory for Lingnan Modern Agriculture
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Abstract

Endoplasmic reticulum autophagy (ER-phagy) is an emerging form of selective autophagy that maintains ER homeostasis by selectively delivering ER components to lysosomes for degradation. Increasing evidence indicates that ER-phagy is closely involved in immune regulation, particularly in the context of viral infection, where it influences host antiviral defenses and virus–host interactions. In this review, we summarize recent advances in ER-phagy research, focusing on the identified mammalian ER-phagy receptors, their molecular characteristics, and their roles in maintaining ER function. Furthermore, we discuss the bidirectional interplay between ER-phagy and viral infections, including how ER-phagy contributes to innate immune responses through the regulation of antiviral signaling pathways, and how viruses manipulate ER-phagy machinery to promote their replication or evade host immunity. By highlighting the immunological significance of ER-phagy in virus–host interactions, this review provides new perspectives on the role of ER quality control mechanisms in antiviral immunity and their potential implications for the development of antiviral strategies.

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Cite

BibTeXRIS
BibTeX
@article{he2026advances,
  title = {{Advances in endoplasmic reticulum autophagy and its role in viral infection}},
  author = {Yulin He and Yaxing Su and Qing Xu and Zhibiao Bian and Pinpin Chu and Chunling Li and Shao-lun Zhai and Yan Li and Zhiyong Jiang and Xia Zhou and Hongchao Gou and Huahua Kang},
  journal = {Frontiers in Immunology},
  year = {2026},
  month = oct,
  doi = {10.3389/fimmu.2026.1966606},
  url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.1966606/full},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Advances in endoplasmic reticulum autophagy and its role in viral infection
AU  - Yulin He
AU  - Yaxing Su
AU  - Qing Xu
AU  - Zhibiao Bian
AU  - Pinpin Chu
AU  - Chunling Li
AU  - Shao-lun Zhai
AU  - Yan Li
AU  - Zhiyong Jiang
AU  - Xia Zhou
AU  - Hongchao Gou
AU  - Huahua Kang
PY  - 2026
DA  - 2026/10/28
JO  - Frontiers in Immunology
DO  - 10.3389/fimmu.2026.1966606
UR  - https://www.frontiersin.org/articles/10.3389/fimmu.2026.1966606/full
AB  - Endoplasmic reticulum autophagy (ER-phagy) is an emerging form of selective autophagy that maintains ER homeostasis by selectively delivering ER components to lysosomes for degradation. Increasing evidence indicates that ER-phagy is closely involved in immune regulation, particularly in the context of viral infection, where it influences host antiviral defenses and virus–host interactions. In this review, we summarize recent advances in ER-phagy research, focusing on the identified mammalian ER-phagy receptors, their molecular characteristics, and their roles in maintaining ER function. Furthermore, we discuss the bidirectional interplay between ER-phagy and viral infections, including how ER-phagy contributes to innate immune responses through the regulation of antiviral signaling pathways, and how viruses manipulate ER-phagy machinery to promote their replication or evade host immunity. By highlighting the immunological significance of ER-phagy in virus–host interactions, this review provides new perspectives on the role of ER quality control mechanisms in antiviral immunity and their potential implications for the development of antiviral strategies.
SN  - 1664-3224
ER  -