Taguchi F, Matsuyama S, Saeki K
National Institute of Neuroscience, NCNP, Kodaira, Tokyo, Japan.
Arch Virol. 1999;144(10):2041-9. doi: 10.1007/s007050050725.
Mouse hepatitis virus (MHV) utilizes a mouse biliary glycoprotein (Bgp) as a receptor. Co-cultivation of MHV-nonpermissive hamster BHK cells devoid of mouse Bgp with mouse DBT cells infected with MHV-A59 or JHMV induces syncytia formation on BHK cells (Bgp-independent fusion). This study shows the difference in Bgp-independent fusion activity among various MHV strains. Under a phase contrast microscopy, JHMV (cl-2, sp-4) induced the Bgp-independent syncytia on BHK cells similar to those observed on DBT cells, while such syncytia were not seen with the infection of other MHV strains (MHV-1, MHV-3, MHV-A59, MHV-S, srr7, srr11 and srr18). Tiny syncytia detectable only by immunofluorescence were produced with the latter MHV strains except for srr7 which failed to produce syncytia. MHVs except for srr7 grew in BHK cells after Bgp-independent infection. The Bgp-independent fusion by JHMV was inhibited either by anti-S1 or anti-S2 antibodies. These results showed that the JHMV spike protein had a remarkably high Bgp-independent fusion activity.
小鼠肝炎病毒（MHV）利用小鼠胆汁糖蛋白（Bgp）作为受体。将缺乏小鼠Bgp的MHV非允许性仓鼠BHK细胞与感染了MHV - A59或JHMV的小鼠DBT细胞共同培养，可诱导BHK细胞形成多核巨细胞（不依赖Bgp的融合）。本研究显示了不同MHV毒株之间不依赖Bgp的融合活性差异。在相差显微镜下，JHMV（cl - 2，sp - 4）在BHK细胞上诱导出与在DBT细胞上观察到的类似的不依赖Bgp的多核巨细胞，而感染其他MHV毒株（MHV - 1、MHV - 3、MHV - A59、MHV - S、srr7、srr11和srr18）时未见到此类多核巨细胞。除srr7未产生多核巨细胞外，后几种MHV毒株产生了仅通过免疫荧光可检测到的微小多核巨细胞。除srr7外的MHV毒株在不依赖Bgp的感染后可在BHK细胞中生长。JHMV不依赖Bgp的融合受到抗S1或抗S2抗体的抑制。这些结果表明，JHMV刺突蛋白具有显著高的不依赖Bgp的融合活性。
