Cell surface influenza haemagglutinin can mediate infection by other animal viruses.
Cell surface influenza haemagglutinin can mediate infection by other animal viruses.
复制标题
细胞表面流感血凝素可以介导其他动物病毒的感染。
作者：
S. Fuller;C. H. V. Bonsdorff;Kai Simons
我们使用过滤生长的Madin达比犬肾（MDCK）细胞来探索流感病毒促进继发性病毒感染的机制。水泡性口炎病毒（VSV）和塞姆利基森林病毒（SFV）仅通过这些极化上皮细胞的基底外侧表面而不通过顶端表面感染。先前感染流感病毒使得细胞容易通过任一表面被VSV或SFV感染。在同一个细胞中，允许和限制病毒进入的表面的存在使我们能够确定流感感染如何增强随后的第二种病毒的感染。生物化学和形态学证据表明，顶端表面的流感血凝素通过与其携带唾液酸的包膜蛋白结合而作为重复感染病毒的受体。流感病毒还促进非上皮细胞中的继发性病毒感染;通常对冠状病毒（小鼠肝炎病毒MHV‐A59）感染具有抵抗力的幼仓鼠肾细胞（BHK‐21）可通过血凝素-唾液酸相互作用感染。促进继发性病毒感染仅需要血凝素的唾液酸结合特性，因为未裂解的血凝素也可介导病毒进入。
We have used filter‐grown Madin‐Darby canine kidney (MDCK) cells to explore the mechanism by which influenza virus facilitates secondary virus infection. Vesicular stomatitis virus (VSV) and Semliki Forest virus (SFV) infect only through the basolateral surface of these polarized epithelial cells and not through the apical surface. Prior infection with influenza virus rendered the cell susceptible to infection by VSV or SFV through either surface. The presence of both a permissive and a restrictive surface for virus entry in the same cell allowed us to determine how the influenza infection enhanced the subsequent infection of a second virus. Biochemical and morphological evidence showed that influenza haemagglutinin on the apical surface serves as a receptor for the superinfecting virus by binding to its sialic acid‐bearing envelope proteins. Influenza virus also facilitates secondary virus infection in non‐epithelial cells; baby hamster kidney cells (BHK‐21), which are normally resistant to infection by the coronavirus (mouse hepatitis virus MHV‐A59), could be infected via the haemagglutinin‐sialic acid interaction. Facilitation of secondary virus infection requires only the sialic acid‐binding properties of the haemagglutinin since the uncleaved haemagglutinin could also mediate virus entry.