Chiu Wen-Ling, Lin Chi-Long, Yang Min-Hsiang, Tzou Der-Lii M, Chang Wen
Institute of Molecular Biology, Academia Sinica, Taipei, Taiwan, Republic of China.
J Virol. 2007 Mar;81(5):2149-57. doi: 10.1128/JVI.02302-06. Epub 2006 Dec 13.
Vaccinia virus intracellular mature virus (IMV) binds to glycosaminoglycans (GAGs) on cells via three virion proteins, H3L, A27L, and D8L. In this study, we demonstrated that binding of IMV to BSC40 cells was competitively inhibited by soluble laminin but not by fibronectin or collagen V, suggesting that this cell surface extracellular matrix (ECM) protein may play a role in vaccinia virus entry. Moreover, IMV infection of GAG(-) sog9 cells was also inhibited by laminin, demonstrating that virion binding to laminin does not involve a prior interaction with GAGs. Furthermore, comparative envelope protein analyses of wild-type vaccinia virus strain Western Reserve, which binds to laminin, and of a mutant virus, IA27L, which does not, showed that the A26L open reading frame (ORF), encoding an envelope protein, was mutated in IA27L, resulting in A26L being absent from the IMV. Expression of the wild-type A26L ORF in IA27L resulted in laminin binding activity. Moreover, recombinant A26L protein bound to laminin in vitro with a high affinity, providing direct evidence that A26L is the laminin binding protein on IMV. In summary, these results reveal a novel role for the vaccinia viral envelope protein A26L in binding to the ECM protein laminin, an association that is proposed to facilitate IMV entry.
痘苗病毒细胞内成熟病毒(IMV)通过三种病毒体蛋白H3L、A27L和D8L与细胞上的糖胺聚糖(GAG)结合。在本研究中,我们证明IMV与BSC40细胞的结合受到可溶性层粘连蛋白的竞争性抑制,但不受纤连蛋白或Ⅴ型胶原的抑制,这表明这种细胞表面细胞外基质(ECM)蛋白可能在痘苗病毒进入过程中发挥作用。此外,层粘连蛋白也抑制了GAG(-)sog9细胞的IMV感染,表明病毒体与层粘连蛋白的结合不涉及与GAG的预先相互作用。此外,对与层粘连蛋白结合的野生型痘苗病毒株Western Reserve和不与层粘连蛋白结合的突变病毒IA27L进行包膜蛋白比较分析,结果显示,编码包膜蛋白的A26L开放阅读框(ORF)在IA27L中发生了突变,导致IMV中不存在A26L。在IA27L中表达野生型A26L ORF可产生层粘连蛋白结合活性。此外,重组A26L蛋白在体外与层粘连蛋白具有高亲和力结合,直接证明A26L是IMV上的层粘连蛋白结合蛋白。总之,这些结果揭示了痘苗病毒包膜蛋白A26L在与ECM蛋白层粘连蛋白结合中的新作用,这种结合被认为有助于IMV进入。