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Background <p>Chronic hepatitis B (CHB) with positive HBeAg status constitutes a significant contributor to the development of liver cirrhosis and hepatocellular carcinoma. Pegylated interferon-alpha (pegIFNα) is a common treatment, but its response rate remains limited, and the underlying mechanisms are not fully understood.</p> Methods <p>Eighty-two HBeAg-positive CHB patients were enrolled. miR-194-5p expression, HBeAg, and HBV DNA levels were detected using qRT-PCR, ELISA, and quantitative PCR, respectively. ROC and logistic regression analyses were performed. Cellular experiments, including dual-luciferase reporter and rescue assays, along with Western blot analysis of JAK-STAT pathway proteins, were conducted to verify targeting and function.</p> Results <p>Complete response (CR) patients had significantly lower baseline HBV DNA than suboptimal response (SR) patients. After 48 weeks of pegIFNα therapy, miR-194-5p expression decreased notably in the CR group and correlated positively with HBV DNA and HBeAg levels. miR-194-5p predicted treatment response with an AUC of 0.831 and was an independent predictor. Mechanistically, miR-194-5p targeted SOCS2. Functional studies demonstrated that miR-194-5p overexpression enhanced, while SOCS2 supplementation attenuated, pegIFNα-induced phosphorylation of STAT1/STAT2, thereby influencing cell viability and inflammatory factor expression (TNF-α, IL-6, IL-1β).</p> Conclusion <p>miR-194-5p may predict pegIFNα response in HBeAg-positive CHB. It regulates interferon signaling by targeting SOCS2 and modulating the JAK-STAT pathway activation, suggesting the miR-194-5p/SOCS2 axis as a potential therapeutic target.</p>

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miR-194-5p targets SOCS2 to predict pegIFNα treatment response in HBeAg-positive chronic hepatitis B patients

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月5日

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  • Yanling Chen,
  • LijuanZhang,
  • Lihua Ling

摘要

Background

Chronic hepatitis B (CHB) with positive HBeAg status constitutes a significant contributor to the development of liver cirrhosis and hepatocellular carcinoma. Pegylated interferon-alpha (pegIFNα) is a common treatment, but its response rate remains limited, and the underlying mechanisms are not fully understood.

Methods

Eighty-two HBeAg-positive CHB patients were enrolled. miR-194-5p expression, HBeAg, and HBV DNA levels were detected using qRT-PCR, ELISA, and quantitative PCR, respectively. ROC and logistic regression analyses were performed. Cellular experiments, including dual-luciferase reporter and rescue assays, along with Western blot analysis of JAK-STAT pathway proteins, were conducted to verify targeting and function.

Results

Complete response (CR) patients had significantly lower baseline HBV DNA than suboptimal response (SR) patients. After 48 weeks of pegIFNα therapy, miR-194-5p expression decreased notably in the CR group and correlated positively with HBV DNA and HBeAg levels. miR-194-5p predicted treatment response with an AUC of 0.831 and was an independent predictor. Mechanistically, miR-194-5p targeted SOCS2. Functional studies demonstrated that miR-194-5p overexpression enhanced, while SOCS2 supplementation attenuated, pegIFNα-induced phosphorylation of STAT1/STAT2, thereby influencing cell viability and inflammatory factor expression (TNF-α, IL-6, IL-1β).

Conclusion

miR-194-5p may predict pegIFNα response in HBeAg-positive CHB. It regulates interferon signaling by targeting SOCS2 and modulating the JAK-STAT pathway activation, suggesting the miR-194-5p/SOCS2 axis as a potential therapeutic target.