Gallagher T M
Department of Microbiology and Immunology, Loyola University Medical Center, Maywood, Illinois 60153, USA.
Adv Exp Med Biol. 1995;380:331-6.
The intracellular interaction of the coronavirus mouse hepatitis virus (MHV) with its cellular receptor (MHVR) was investigated. Overexpression of MHVR from vaccinia vectors during an ongoing MHV infection resulted in dramatic inhibition of virus production. Infectivity in both cytoplasmic extracts and supernatants was reduced by over three orders of magnitude relative to control cultures in which a truncated MHVR lacking virus binding activity was expressed. Complete MHV virions were not detectable in supernatants of MHVR expressing cells. In the presence of overexpressed MHVR, the coronavirus spike protein was not cleaved into posttranslation products S1 and S2, nor was it fully processed into a form resistant to endoglycosidase H digestion, indicating that intracellular engagement of spike with receptor prevented spike transport and consequent association with virions.
对冠状病毒小鼠肝炎病毒(MHV)与其细胞受体(MHVR)的细胞内相互作用进行了研究。在持续的MHV感染过程中,痘苗载体过量表达MHVR导致病毒产生受到显著抑制。相对于表达缺乏病毒结合活性的截短MHVR的对照培养物,细胞质提取物和上清液中的感染性降低了三个数量级以上。在表达MHVR的细胞上清液中未检测到完整的MHV病毒粒子。在过量表达MHVR的情况下,冠状病毒刺突蛋白未被切割成翻译后产物S1和S2,也未被完全加工成对内切糖苷酶H消化具有抗性的形式,这表明刺突与受体的细胞内结合阻止了刺突的转运以及随后与病毒粒子的结合。