Rodriguez J E, Loepfe T R, Swack N S
Arch Virol. 1987;94(3-4):177-89. doi: 10.1007/BF01310712.
Human cytomegalovirus induced beta interferon in cultures of human foreskin cells. The inhibitor was first released between 8 and 16 hours after infection, about 48 hours before progeny virus. In cultures infected with low concentrations of virus, interferon was produced as the infection spread, and then in amounts larger than expected. After infection with cytomegalovirus, cells which had been primed for 48 hours with purified beta interferon produced significantly more interferon than unprimed cells, and the interferon was produced earlier, between 2 and 8 hours after infection. CMV-induced interferon also was able to prime cells. The data suggest that the relatively large quantities of interferon detected in cultures infected with low concentrations of cytomegalovirus result from endogenous priming: those cells infected early first produce interferon which primes uninfected cells, then virus which induces the primed cells to produce interferon in relatively high concentrations.
人巨细胞病毒在人包皮细胞培养物中诱导β干扰素产生。该抑制剂在感染后8至16小时首次释放，比子代病毒出现早约48小时。在低浓度病毒感染的培养物中，随着感染扩散产生干扰素，且产生量比预期的多。用纯化的β干扰素预处理48小时的细胞在感染巨细胞病毒后，产生的干扰素比未预处理的细胞显著更多，且干扰素在感染后2至8小时更早产生。巨细胞病毒诱导的干扰素也能够预处理细胞。数据表明，在低浓度巨细胞病毒感染的培养物中检测到的相对大量的干扰素是内源性预处理的结果：那些早期感染的细胞首先产生干扰素，该干扰素预处理未感染的细胞，然后病毒诱导经预处理的细胞产生相对高浓度的干扰素。
