Okada M, Minamishima Y
Department of Microbiology, Miyazaki Medical College.
Microbiol Immunol. 1987;31(5):435-47. doi: 10.1111/j.1348-0421.1987.tb03106.x.
Host-mediated antiviral effect of 2 biological response modifiers (BRM), OK-432, and PS-K, against murine cytomegalovirus (MCMV) was evaluated in chronically or latently infected mice. In the early stage of chronic MCMV infection, the BRM-induced resistance was evidenced by decrease in infectious viruses replicated in the salivary glands and by augmented cytotoxic activity of the spleen cells against YAC-1 cells and MCMV-infected mouse embryonic fibroblasts (MEF). In the late stage of chronic MCMV infection, the BRM treatment did not eliminate MCMV from the mice, but did prevent exacerbation of MCMV infection in the salivary glands induced by administration of cyclophosphamide (CY). In mice latently infected by MCMV, BRM treatment suppressed CY-induced reactivation of MCMV in the salivary glands. It was suggested that the antiviral effect of BRM against MCMV in chronically or latently infected mice was based on activation of natural killer (NK) cells and cytotoxic T lymphocytes (CTL).
在慢性或潜伏感染的小鼠中评估了两种生物反应调节剂(BRM)——OK-432和PS-K对鼠巨细胞病毒(MCMV)的宿主介导抗病毒作用。在慢性MCMV感染的早期,BRM诱导的抗性表现为唾液腺中复制的感染性病毒减少,以及脾细胞对YAC-1细胞和MCMV感染的小鼠胚胎成纤维细胞(MEF)的细胞毒性活性增强。在慢性MCMV感染的后期,BRM治疗并未从小鼠体内清除MCMV,但确实预防了环磷酰胺(CY)给药诱导的唾液腺MCMV感染的加重。在MCMV潜伏感染的小鼠中,BRM治疗抑制了CY诱导的唾液腺中MCMV的重新激活。有人提出,BRM对慢性或潜伏感染小鼠中MCMV的抗病毒作用基于自然杀伤(NK)细胞和细胞毒性T淋巴细胞(CTL)的激活。