Scheffler P, Haghchenas D, Wigand R
Acta Virol. 1975 Apr;19(2):106-15.
The multiplication of adenovirus 19 in HeLa cells was inhibited by various purine and pyrimidine analogues and by virazole. The formation of infectious virus and of capsid proteins (haemagglutin, group-specific complement-fixing antigen) was inhibited to the same degree, while the viral cytopathic effect (CPE) was not inhibited. The reversibility of the inhibition after removal of the substances was more complete for purine than for pyrimidine analogues. The inhibition was counteracted by simulataneous addition of the corresponding nucleosides. Adenosine was more effected than guanosine against purine analogues; both were partially effective against virazole, but none of them against arabinofuranosyladenine. The time-dependence of inhibition, the ensuing eclipse period after removal of the inhibitors, and the successive application of two inhibitors led to the conclusion that most of them affect the viral multiplication mainly by inhibition of DNA synthesis. Azacytidine inhibits the synthesis of structural proteins as well.
19型腺病毒在HeLa细胞中的增殖受到多种嘌呤和嘧啶类似物以及病毒唑的抑制。传染性病毒和衣壳蛋白(血凝素、群特异性补体结合抗原)的形成受到同等程度的抑制,而病毒细胞病变效应(CPE)未受抑制。去除物质后,嘌呤类似物的抑制作用比嘧啶类似物更易完全逆转。同时添加相应核苷可抵消这种抑制作用。腺苷对嘌呤类似物的作用比鸟苷更明显;两者对病毒唑均有部分作用,但对阿糖腺苷均无作用。抑制作用的时间依赖性、去除抑制剂后随之出现的隐蔽期以及两种抑制剂的连续应用得出结论,大多数抑制剂主要通过抑制DNA合成来影响病毒增殖。阿扎胞苷也抑制结构蛋白的合成。