行业焦点

图1 ASFV I73R抑制宿主蛋白合成的示意图

该研究得到国家自然科学基金（32170161；U19A2039；U20A2059；32102652）、国家重点研发专项（2021YFD1801401；2021YFD1801300；2021YFD1800104）、上海市青年科技英才杨帆计划（23YF1457400）、中国农业科学院农业科学技术创新项目（CAAS-ZDRW202203）和中央公益性科研单位基础研究基金（Y2022PT11）等项目资助。上海兽医研究所刘英楠博士和华中农业大学沈洲博士为论文共同第一作者，上海兽医研究所陈鸿军研究员、华中农业大学彭贵青教授和华南农业大学王衡副教授为论文共同通讯作者。

审核：彭贵青

【英文摘要】

African swine fever virus (ASFV) is a large, double-stranded DNA virus that causes a fatal disease in pigs, posing a threat to the global pig industry. Whereas some ASFV proteins have been found to play important roles in ASFV-host interaction, the functional roles of many proteins are still largely unknown. In this study, we identified I73R, an early viral gene in the replication cycle of ASFV, as a key virulence factor. Our findings demonstrate that pI73R suppresses the host innate immune response by broadly inhibiting the synthesis of host proteins, including antiviral proteins. Crystallization and structural characterization results suggest that pI73R is a nucleic-acid-binding protein containing a Zα domain. It localizes in the nucleus and inhibits host protein synthesis by suppressing the nuclear export of cellular messenger RNA (mRNAs). While pI73R promotes viral replication, the deletion of the gene showed that it is a nonessential gene for virus replication. In vivo safety and immunogenicity evaluation results demonstrate that the deletion mutant ASFV-GZΔI73R is completely nonpathogenic and provides effective protection to pigs against wild-type ASFV. These results reveal I73R as a virulence-related gene critical for ASFV pathogenesis and suggest that it is a potential target for virus attenuation. Accordingly, the deletion mutant ASFV-GZΔI73R can be a potent live-attenuated vaccine candidate

原文链接：https://pubmed.ncbi.nlm.nih.gov/37023125/

https://pubmed.ncbi.nlm.nih.gov/33328305/