Special Issue: “Updates on HBV Infection”

Chemin, Isabelle; Pujol, Flor H.

doi:10.3390/microorganisms10030580

Cited by 4 publications

(2 citation statements)

References 24 publications

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“…Hepatitis B virus (HBV) remains a global public health problem, with approximately 296 million people chronically infected and 1.5 million new cases diagnosed each year 1 . Chronic hepatitis B (CHB) leads to a wide range of complications, including severe hepatitis, cirrhosis, liver cancer, and even death 2,3 .…”

Section: Introductionmentioning

confidence: 99%

“…approximately 296 million people chronically infected and 1.5 million new cases diagnosed each year. 1 Chronic hepatitis B (CHB) leads to a wide range of complications, including severe hepatitis, cirrhosis, liver cancer, and even death. 2,3 Activation of innate immunity is the firstline of defense against virus infection, leading to the production of type I interferons (IFN-Is).…”

mentioning

confidence: 99%

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Autophagy‐related protein 5 (ATG5) interacts with bone marrow stromal cell antigen 2 (BST2) to stimulate HBV replication through antagonizing the antiviral activity of BST2

Li,

Wen,

Wang

et al. 2024

Journal of Medical Virology

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Hepatitis B virus (HBV) infection is a major global health burden with 820 000 deaths per year. In our previous study, we found that the knockdown of autophagy‐related protein 5 (ATG5) significantly upregulated the interferon‐stimulated genes (ISGs) expression to exert the anti‐HCV effect. However, the regulation of ATG5 on HBV replication and its underlying mechanism remains unclear. In this study, we screened the altered expression of type I interferon (IFN‐I) pathway genes using RT² Profiler™ PCR array following ATG5 knock‐down and we found the bone marrow stromal cell antigen 2 (BST2) expression was significantly increased. We then verified the upregulation of BST2 by ATG5 knockdown using RT‐qPCR and found that the knockdown of ATG5 activated the Janus kinase/signal transducer and activator of transcription (JAK‐STAT) signaling pathway. ATG5 knockdown or BST2 overexpression decreased Hepatitis B core Antigen (HBcAg) protein, HBV DNA levels in cells and supernatants of HepAD38 and HBV‐infected NTCP‐HepG2. Knockdown of BST2 abrogated the anti‐HBV effect of ATG5 knockdown. Furthermore, we found that ATG5 interacted with BST2, and further formed a ternary complex together with HBV‐X (HBx). In conclusion, our finding indicates that ATG5 promotes HBV replication through decreasing BST2 expression and interacting with it directly to antagonize its antiviral function.

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Section: Introductionmentioning

confidence: 99%

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confidence: 99%