Sroller V, Kutinová L, Nĕmecková S, Simonová V, Vonka V
Institute of Hematology and Blood Transfusion, Praha, Czech Republic.
Arch Virol. 1998;143(7):1311-20. doi: 10.1007/s007050050377.
3-beta-Hydroxysteroid dehydrogenase (3-beta-HSD) activity coded for by the A44L gene of vaccinia virus (VV) was demonstrated in CV-1 cultures infected by all five VV strains tested, viz. WR, Praha virus, DRYVAX Wyeth-derived virus (DD), LIVP and MVA. Deletion of the A44L gene in two Praha virus-derived clones (the moderately virulent P13 and the highly attenuated P20), the WR and DD viruses resulted in absence of 3-beta-HSD activity from infected cultures. The virulence for mice of P13 was not affected, and that of WR was only slightly decreased, by the A44L gene deletion. Recombinant VVs expressing either varicella-zoster virus glycoprotein E (VZV-gE) or hepatitis B virus preS2-S protein (HBV-preS2-S) and their respective A44L deleted mutants were used in immunogenicity tests in mice. In terms of antibody response to VV and the recombinant proteins, the deletion resulted in a lowering the immunogenicity in the moderately virulent clone P13 virus and its progenies. In the highly attenuated P20 and DD viruses and their progenies no effects were apparent.
在受测试的所有五种痘苗病毒（VV）毒株感染的CV-1培养物中，均证实了痘苗病毒（VV）A44L基因编码的3-β-羟基类固醇脱氢酶（3-β-HSD）活性，这五种毒株分别是WR、布拉格病毒、惠氏来源的DRYVAX病毒（DD）、LIVP和MVA。在两个源自布拉格病毒的克隆（中等毒力的P13和高度减毒的P20）、WR和DD病毒中删除A44L基因，导致受感染培养物中缺乏3-β-HSD活性。A44L基因缺失对P13对小鼠的毒力没有影响，对WR的毒力仅略有降低。表达水痘-带状疱疹病毒糖蛋白E（VZV-gE）或乙型肝炎病毒前S2-S蛋白（HBV-preS2-S）的重组痘苗病毒及其各自缺失A44L的突变体用于小鼠免疫原性测试。就对痘苗病毒和重组蛋白的抗体反应而言，缺失导致中等毒力克隆P13病毒及其子代的免疫原性降低。在高度减毒的P20和DD病毒及其子代中，没有明显影响。
