慢性乙型肝炎(CHB)患者干扰素-α(IFN-α)疗效的个体差异局限了IFN-α的临床应用，从宿主角度寻找新的疗效预测指标并深入研究其作用机制具有重要意义。研究表明干扰素刺激基因TRIM22能激活NF-κB信号通路发挥抗病毒作用，课题组前期发现miR-548c可显著降低TRIM22表达，且两者在IFN-α治疗不同应答组的CHB患者外周血样本中呈负相关。由此，我们提出假说：CHB患者相关转录因子突变引起miR-548c表达差异，调控靶蛋白TRIM22进而调节NF-κB信号通路，最终协同或拮抗IFN-α的抗病毒作用。为验证该假说，我们通过体内外实验探究miR-548c表达差异的上游调控机制，验证miR-548c/TRIM22轴对干扰素疗效的影响，并结合实验室数据评估miR-548c作为IFN-α疗效预测指标的价值。本研究有望为临床开展个体化治疗提供新的实验依据，丰富和发展CHB的精准治疗。

Individual differences in the efficacy of interferon-α (IFN-α) have limited the clinical application of IFN-α in patients with chronic hepatitis B (CHB). It is of great significance to find new predictive indicators of efficacy and to study its mechanism from the perspective of the host. Studies have shown that the interferon-stimulated gene TRIM22 can activate the NF-κB signaling pathway to play an antiviral role. Our research group previously found that miR-548c can significantly reduce TRIM22 expression, and a negative correlation between these two was found in peripheral blood samples of CHB patients with different response groups treated with IFN-α. Therefore, we propose a hypothesis that mutations in related transcription factors in patients with CHB cause differential expression of miR-548c, modulate the target protein TRIM22 and thereby regulate the NF-κB signaling pathway, and ultimately synergize or antagonize the antiviral effect of IFN-α. To test this hypothesis, we will explore the upstream regulatory mechanism of miR-548c differential expression through in vivo and in vitro experiments, verify the effect of miR-548c/TRIM22 on the efficacy of interferon, and eventually combine laboratory data to evaluate the value of miR-548c as a predictor of IFN-α efficacy. This study is expected to provide a new experimental basis for the clinical development of individualized treatment, and to enrich and develop precision treatment of CHB.