CREG1 restricts ALV-J replication via the mitochondrial dysfunction–driven activation of innate immunity and apoptosis Article Swipe
Qihong Zhang
,
Min Wang
,
Min‐Hsiung Pan
,
Ji-Wen Xia
,
Tao Xu
,
Wen Luo
,
Xiquan Zhang
·
YOU?
·
· 2025
· Open Access
·
· DOI: https://doi.org/10.1101/2025.08.18.670803
YOU?
·
· 2025
· Open Access
·
· DOI: https://doi.org/10.1101/2025.08.18.670803
Despite the implementation of purification strategies to partially limit J subgroup avian leukosis virus (ALV-J) infection, the involvement of host factors in the underlying infection mechanism remains largely undefined. Here, we identify cellular repressor of E1A-stimulated genes 1 (CREG1) as a key regulator of mitochondrial function and a critical immune-related gene involved in ALV-J infection. The objective of this study was to explore the effects and underlying mechanisms of CREG1 in the context of ALV-J infection. Overexpression of CREG1 upregulates the expression of type I interferon (I-IFN) and certain interferon-stimulated genes (ISGs), thereby suppressing viral replication. Mechanistically, overexpression of CREG1 induces mitochondrial dysfunction, characterized by a decrease in mitochondrial membrane potential (Δψm), reduced adenosine triphosphate (ATP) production and respiratory chain activity, enhanced mitophagy, and increased release of mitochondrial DNA (mtDNA), which in turn triggers the activation of innate immune responses. Mitochondrial dysfunction further leads to the cytosolic release of cytochrome c and an increase in reactive oxygen species (ROS) levels, thereby triggering a robust apoptotic response. Moreover, the regulation of mitochondrial function by CREG1 depends on its interaction with the mitochondrial chaperone protein heat shock protein 1 (HSPD1), and their co-expression synergistically amplifies the antiviral response. In this study, we identify CREG1 as a potent antiviral gene and underscore the pivotal roles of mitochondria-mediated innate immunity and apoptosis during ALV-J infection. Author summary Despite efforts to limit J subgroup avian leukosis virus (ALV-J) infection, the role of host factors in the infection process is still not fully understood. In this study, we highlight the cellular repressor of E1A-stimulated genes 1 (CREG1) as a crucial regulator of mitochondrial function and immune responses during ALV-J infection. We show that CREG1 overexpression enhances type I interferon (I-IFN) and interferon-stimulated genes (ISGs) expression, inhibiting viral replication. This is achieved through mitochondrial dysfunction, including reduced mitochondrial membrane potential, lower ATP production, and increased mitophagy and mitochondrial DNA release, which activate innate immunity. CREG1-induced mitochondrial dysfunction also triggers apoptosis by releasing cytochrome c and increasing reactive oxygen species (ROS). Furthermore, CREG1 interacts with heat shock protein 1 (HSPD1) to amplify its antiviral effects. Our findings establish CREG1 as a key antiviral gene and emphasize the importance of mitochondrial-mediated immune responses and apoptosis in ALV-J infection.
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- Type
- preprint
- Language
- en
- Landing Page
- https://doi.org/10.1101/2025.08.18.670803
- https://www.biorxiv.org/content/biorxiv/early/2025/08/22/2025.08.18.670803.full.pdf
- OA Status
- green
- References
- 69
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W4413427976
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W4413427976Canonical identifier for this work in OpenAlex
- DOI
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https://doi.org/10.1101/2025.08.18.670803Digital Object Identifier
- Title
-
CREG1 restricts ALV-J replication via the mitochondrial dysfunction–driven activation of innate immunity and apoptosisWork title
- Type
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preprintOpenAlex work type
- Language
-
enPrimary language
- Publication year
-
2025Year of publication
- Publication date
-
2025-08-22Full publication date if available
- Authors
-
Qihong Zhang, Min Wang, Min‐Hsiung Pan, Ji-Wen Xia, Tao Xu, Wen Luo, Xiquan ZhangList of authors in order
- Landing page
-
https://doi.org/10.1101/2025.08.18.670803Publisher landing page
- PDF URL
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https://www.biorxiv.org/content/biorxiv/early/2025/08/22/2025.08.18.670803.full.pdfDirect link to full text PDF
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YesWhether a free full text is available
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-
greenOpen access status per OpenAlex
- OA URL
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https://www.biorxiv.org/content/biorxiv/early/2025/08/22/2025.08.18.670803.full.pdfDirect OA link when available
- Concepts
-
Innate immune system, Replication (statistics), Apoptosis, Cell biology, Immunity, Biology, Virology, Immunology, Genetics, Immune systemTop concepts (fields/topics) attached by OpenAlex
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0Total citation count in OpenAlex
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69Number of works referenced by this work
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10Other works algorithmically related by OpenAlex
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