4月12日，河南农业大学动物医学院褚贝贝课题组在Microbiology Spectrum上发表了题为：EGCG restricts PRRSV proliferation by disturbing lipid metabolism的研究论文，详细解析了EGCG抑制脂质合成和PRRSV感染的分子机制。
猪繁殖与呼吸综合征病毒（PRRSV）感染导致猪晚期繁殖衰竭和呼吸系统疾病，严重影响全球养猪业。已有一些脂质参与PRRSV增殖的相关报道。褚贝贝课题组前期研究结果表明，PRRSV通过下调NDRG1表达激活脂噬，促进病毒复制。因此，脂质代谢关键分子有望成为PRRSV防控的药物靶标。
EGCG是绿茶中含量最丰富的儿茶素，具有多种生物学功能，包括抗肿瘤、抗炎和免疫调节作用。作者们首先检测了EGCG对胞活力、细胞周期和凋亡的影响。结果表明EGCG对猪肺泡巨噬细胞和MARC-145细胞的细胞活力、细胞周期进程和凋亡没有显著影响。用EGCG处理猪肺泡巨噬细胞和MARC-145细胞能够在体外显著抑制高致病性和低致病性PRRSV的复制。
为了深入揭示EGCG抑制PRRSV感染的分子机制，作者们检测了EGCG对PRRSV生活周期的影响。结果表明EGCG抑制PRRSV的复制和组装，但不影响病毒的吸附、进入和释放。虽然PRRSV感染能够促进细胞中脂滴形成和脂质含量，但是EGCG显著逆转这一表型。进一步证明EGCG抑制PRRSV诱导的脂质合成关键酶的表达。此外，EGCG还能抑制PRRSV激活的脂噬。在EGCG处理条件下，给细胞补加油酸能够恢复PRRSV的复制和组装。以上研究结果表明，EGCG通过扰乱脂质代谢抑制PRRSV增殖。
硕士研究生于鹏伟为本文的第一作者。这项研究获得了国家自然科学基金等项目的资助。
Abstract
Porcine reproductive and respiratory syndrome virus (PRRSV) infection leads to late-term reproductive failure and respiratory illness that affect the global swine industry. Epigallocatechin gallate (EGCG) is a polyphenolic compound from green tea that exerts antiviral activity against diverse viruses. This study aimed to report an uncharacterized mechanism of how EGCG restricted PRRSV proliferation. EGCG showed no significant effects on cell viability, cell cycle progression, and apoptosis in porcine alveolar macrophages and MARC-145 cells. The treatment of cells with EGCG attenuated the replication of both highly pathogenic and less pathogenic PRRSV in vitro. The viral life cycle analysis demonstrated that EGCG affected PRRSV replication and assembly, but not viral attachment, entry, or release. Interestingly, EGCG treatment abrogated the increased lipid droplets formation and lipid content induced by PRRSV infection. We further demonstrated that EGCG blocked PRRSV-stimulated expression of the key enzymes in lipid synthesis. In addition, EGCG attenuated PRRSV-induced autophagy that is critical for PRRSV proliferation. The supplementation of oleic acid restored PRRSV replication and assembly under EGCG treatment. Together, our results support that EGCG inhibits PRRSV proliferation through disturbing lipid metabolism.
本期编辑：horizon
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