Metzger B, Podlech J, Müller S, Falke D
Division of Experimental Virology, Johannes Gutenberg University, Mainz, Federal Republic of Germany.
Arch Virol. 1988;99(3-4):143-52. doi: 10.1007/BF01311065.
Suppression of humoral antibody formation against HSV is not only induced by replicating Herpes simplex virus type 2 (HSV-2) but also by the defective strain ANG and the deletion mutant 1301 of Herpes simplex virus type 1 (HSV-1). Moreover, ts-mutants A, H, K, S, 1201 and 1208 of HSV-1 as well as some ts-mutants of HSV-2 and "defective-interfering" particles of HSV-1 after high multiplicity of infection-passages induced suppression. Treatment of infected mice with ACG reduced antibody-formation but did not result in suppression. UV-irradiation of the antibody producing strain Len of HSV-1 strongly reduces antibody formation and induces suppression. Experiments using a series of intertypic recombinants showed the suppressing activity to be spread over the whole genome of HSV-2. It is concluded that suppression is induced by more than one region of the genome of HSV-2 and by incomplete replication of HSV-1 and 2.
针对单纯疱疹病毒(HSV)的体液抗体形成抑制不仅可由复制性2型单纯疱疹病毒(HSV-2)诱导,也可由缺陷株ANG和1型单纯疱疹病毒(HSV-1)的缺失突变体1301诱导。此外,HSV-1的温度敏感突变体A、H、K、S、1201和1208,以及HSV-2的一些温度敏感突变体和高感染复数传代后的HSV-1“缺陷干扰”颗粒也可诱导抑制。用阿昔洛韦治疗感染小鼠可减少抗体形成,但不会导致抑制。对HSV-1抗体产生株Len进行紫外线照射可强烈减少抗体形成并诱导抑制。使用一系列型间重组体的实验表明,抑制活性分布于HSV-2的整个基因组。得出的结论是,抑制是由HSV-2基因组的多个区域以及HSV-1和HSV-2的不完全复制诱导的。