Matis J, Krivjanská M
Institute of Virology, Slovak Academy of Sciences, Bratislava, Czechoslovakia.
Acta Virol. 1991 Jan;35(1):44-53.
Synthesis of the major DNA-binding protein (ICP8) was investigated in primary rabbit kidney (RK) and Vero cells infected with the syncytial (syn) strain HSZP or with the non-syn strain KOS of herpes simplex virus type 1 (HSV-1). Results showed the following: 1. In contrast to strain KOS, the rate of viral polypeptide synthesis was accelerated in Vero cells infected with strain HSZP. The ICP8 could be detected in the nuclei of cells by one hour post-infection (hr p. i.) where it became associated with the viral DNA (DNase sensitive form). Later on (7 hr p.i.), the synthesis of viral polypeptides decreased and no further translocation of ICP8 from the cytoplasm into the nucleus was observed. 2. Strain HSZP was approx. three times more resistant to the action of phosphonoacetic acid (PAA) than strain KOS. In order to block the synthesis of HSZP gamma-2 polypeptides, a concentration of 600 micrograms PAA/ml had to be used. Under this condition, the HSZP ICP8 was translocated into the cell nucleus at later interval only (7 hr p.i.), and it was still possible to release this polypeptide from the nucleus by DNase treatment. The failure of the HSZP ICP8 to associate with the nuclear matrix (DNase resistant form) of infected cells in the absence of viral DNA replication may reflect its predominant affinity for the viral DNA which, in turn, may be responsible for the observed accelerated synthesis of the HSZP polypeptides in infected Vero cells. 3. In primary RK cells infected with strain HSZP the ICP8 did not translocate into the cell nucleus. Therefore, no gamma-2 polypeptides were synthesized.
研究了在感染1型单纯疱疹病毒(HSV-1)的合胞体(syn)株HSZP或非合胞体株KOS的原代兔肾(RK)细胞和Vero细胞中主要DNA结合蛋白(ICP8)的合成情况。结果如下:1. 与KOS株相比,感染HSZP株的Vero细胞中病毒多肽合成速率加快。感染后1小时(h p.i.)即可在细胞核中检测到ICP8,此时它与病毒DNA(对脱氧核糖核酸酶敏感的形式)结合。随后(感染后7小时),病毒多肽合成减少,未观察到ICP8从细胞质进一步转运到细胞核。2. HSZP株对膦甲酸(PAA)作用的抗性约为KOS株的三倍。为了阻断HSZPγ-2多肽的合成,必须使用600微克/毫升的PAA浓度。在此条件下,HSZP ICP8仅在较晚时间间隔(感染后7小时)转运到细胞核中,并且仍可通过脱氧核糖核酸酶处理从细胞核中释放该多肽。在没有病毒DNA复制的情况下,HSZP ICP8未能与感染细胞的核基质(对脱氧核糖核酸酶有抗性的形式)结合,这可能反映了它对病毒DNA的主要亲和力,而这反过来可能是感染的Vero细胞中观察到的HSZP多肽合成加速的原因。3. 在感染HSZP株的原代RK细胞中,ICP8未转运到细胞核中。因此,未合成γ-2多肽。