Baker P N, Bradshaw T K, Morser J, Burke D C
J Gen Virol. 1979 Oct;45(1):177-84. doi: 10.1099/0022-1317-45-1-177.
5-Bromodeoxyuridine (BrdUrd) increased interferon production by the Namalwa line of human lymphoblastoid cells treated with Sendai virus, but inhibited their growth. Thymidine, which also inhibited cell growth had no effect on interferon production, so that growth inhibition per se was not the cause of the stimulation. BrdUrd was incorporated into cellular DNA; 5-chlorodeoxyuridine and 5-iododeoxyuridine (which are also incorporated) increased the interferon yield, but 5-fluorodeoxyuridine (which is not incorporated) did not. Thymidine reduced both the incorporation of BrdUrd and its stimulatory effect on interferon production. Deoxycytidine (which prevents the cytotoxic effects of BrdUrd) had no effect on the stimulation. BrdUrd also stimulated interferon production in response to poly(rI) . poly(rC) in growing human diploid fibroblasts but not in SV40 virus-transformed human cells. Since BrdUrd was incorporated into the DNA of all these cells, we concluded that incorporation is necessary, but not sufficient for the stimulation of interferon formation.
5-溴脱氧尿苷(BrdUrd)可增加经仙台病毒处理的Namalwa人淋巴母细胞系的干扰素产量,但会抑制其生长。胸腺嘧啶核苷同样会抑制细胞生长,却对干扰素产生没有影响,所以生长抑制本身并非刺激产生的原因。BrdUrd被整合到细胞DNA中;5-氯脱氧尿苷和5-碘脱氧尿苷(同样会被整合)可提高干扰素产量,但5-氟脱氧尿苷(不会被整合)则没有此作用。胸腺嘧啶核苷既能减少BrdUrd的整合,也能降低其对干扰素产生的刺激作用。脱氧胞苷(可防止BrdUrd的细胞毒性作用)对这种刺激没有影响。BrdUrd还能刺激生长中的人二倍体成纤维细胞对聚肌苷酸-聚胞苷酸(poly(rI).poly(rC))产生干扰素,但对SV40病毒转化的人细胞则无此作用。由于BrdUrd被整合到所有这些细胞的DNA中,我们得出结论,整合是刺激干扰素形成所必需的,但并非充分条件。