Sarmiento M, Haffey M, Spear P G
J Virol. 1979 Mar;29(3):1149-58. doi: 10.1128/JVI.29.3.1149-1158.1979.
Experiments done with a temperature"sensitive mutant of herpes simplex virus type 1 (HSV-1) have revealed that one of the virisn glycoproteins, designated VP7(B2), is apparently not required for the production of enveloped virus particles, whereas it does play a critical role in virion infectivity. The mutant, designated HSV-1[HFEM]tsB5, fails to accumulate VP7(B2) at nonpermissive temperature and produces virions that lack detectable quantities of this glycoprotein and that have very low specific infectivity. The poor infectivity of the virions is most readily explained by failure of penetration into the host cell rather than by failure of adsorption to cells because it was shown that the VP7(B2)-deficient virions can bind to cells and that polyethylene glycol, an agent known to promote membrane fusion, can significantly enhance infectivity of the adsorbed virions.
用1型单纯疱疹病毒(HSV-1)的温度敏感突变体进行的实验表明,病毒的一种糖蛋白,命名为VP7(B2),显然不是产生包膜病毒颗粒所必需的,然而它在病毒粒子感染性方面起着关键作用。该突变体命名为HSV-1[HFEM]tsB5,在非允许温度下不能积累VP7(B2),产生的病毒粒子缺乏可检测量的这种糖蛋白,并且具有非常低的比感染性。病毒粒子感染性差最容易解释为是由于穿透进入宿主细胞失败,而不是由于吸附到细胞失败,因为已表明缺乏VP7(B2)的病毒粒子可以与细胞结合,并且聚乙二醇,一种已知可促进膜融合的试剂,可以显著增强吸附病毒粒子的感染性。