美国洛克菲勒大学Charles M. Rice、纽约大学John T. Poirier等研究人员合作发现，TMEM41B是一种泛黄病毒宿主因子。相关论文于2020年12月8日在线发表在《细胞》杂志上。

为了鉴定黄病毒感染所需的宿主因子，研究人员进行了全基因组功能丧失的CRISPR-Cas9筛选。基于这些结果，研究人员主要确定了TMEM41B和VMP1在病毒复制周期中所起的作用。研究人员对TMEM41B的机理研究表明，所测试的黄病毒科所有成员都需要TMEM41B。研究人员测试了另外12个病毒家族，发现冠状病毒科的SARS-CoV-2也需要TMEM41B进行感染。

值得注意的是，东亚人口中近20％的单核苷酸多态性（SNP）减少了黄病毒感染。根据这些机理研究，研究人员认为TMEM41B会被募集到黄病毒RNA复制复合物中来促进膜弯曲，从而为病毒基因组复制创造一个受保护的环境。

据介绍，黄病毒对人类健康构成持续威胁。这些RNA病毒通过蚊子和蜱虫叮咬传播，并经常引起疾病暴发。

附：英文原文

Title: TMEM41B IS A PAN-FLAVIVIRUS HOST FACTOR

Author: H.-Heinrich Hoffmann, William M. Schneider, Kathryn Rozen-Gagnon, Linde A. Miles, Felix Schuster, Brandon Razooky, Eliana Jacobson, Xianfang Wu, Soon Yi, Charles M. Rudin, Margaret R. MacDonald, Laura K. McMullan, John T. Poirier, Charles M. Rice

Issue&Volume: 2020-12-08

Abstract: Flaviviruses pose a constant threat to human health. These RNA viruses are transmitted by the bite of infected mosquitoes and ticks and regularly cause outbreaks. To identify host factors required for flavivirus infection we performed full-genome loss of function CRISPR-Cas9 screens. Based on these results we focused our efforts on characterizing the roles that TMEM41B and VMP1 play in the virus replication cycle. Our mechanistic studies on TMEM41B revealed that all members of the Flaviviridae family that we tested require TMEM41B. We tested 12 additional virus families and found that SARS-CoV-2 of the Coronaviridae also required TMEM41B for infection. Remarkably, single nucleotide polymorphisms (SNPs) present at nearly twenty percent in East Asian populations reduce flavivirus infection. Based on our mechanistic studies we propose that TMEM41B is recruited to flavivirus RNA replication complexes to facilitate membrane curvature, which creates a protected environment for viral genome replication.

DOI: 10.1016/j.cell.2020.12.005

Source: https://www.cell.com/cell/fulltext/S0092-8674(20)31627-5