Ibusuki K, Minamishima Y
Department of Microbiology, Miyazaki Medical College, Japan.
Nat Immun Cell Growth Regul. 1990;9(2):121-8.
The host-mediated antiviral effect of Chlorella vulgaris extracts (CVE) was evaluated in ICR mice against murine cytomegalovirus (MCMV) infection. Mice treated with 10 mg of CVE on days 3 and 1 before virus challenge survived lethal infection. The protective effect of CVE was shown by a decrease in the infectious viruses replicated in the target organs of CVE-treated ICR mice. CVE also protected mice from histopathological damage to the target organs due to MCMV infection. Both the serum interferon (IFN) level and 2'5'-oligoadenylate (2-5A) synthetase activity were elevated in CVE-treated and MCMV-infected mice, and were higher than those in the control mice. The natural killer (NK) activity of spleen cells, which is otherwise deteriorated by lethal MCMV infection, was remarkably augmented in CVE-treated mice. Neither virocidal nor virostatic activity of CVE on MCMV was seen in vitro. Thus, CVE-induced resistance against MCMV seems to be host-mediated. The protective effect correlated with the augmentation of NK activity of the spleen cells and serum IFN activity, which inhibited replication of MCMV in the target organs and subsequently saved the mice from death.
在ICR小鼠中评估了小球藻提取物(CVE)的宿主介导的抗病毒作用,以抵抗鼠巨细胞病毒(MCMV)感染。在病毒攻击前第3天和第1天用10mg CVE处理的小鼠在致死性感染中存活下来。CVE的保护作用表现为CVE处理的ICR小鼠靶器官中复制的感染性病毒减少。CVE还保护小鼠免受MCMV感染对靶器官造成的组织病理学损伤。在CVE处理并感染MCMV的小鼠中,血清干扰素(IFN)水平和2'5'-寡腺苷酸(2-5A)合成酶活性均升高,且高于对照小鼠。脾脏细胞的自然杀伤(NK)活性在致死性MCMV感染后会恶化,但在CVE处理的小鼠中显著增强。在体外未观察到CVE对MCMV的杀病毒或抑制病毒活性。因此,CVE诱导的对MCMV的抗性似乎是宿主介导的。保护作用与脾脏细胞NK活性和血清IFN活性的增强相关,这抑制了MCMV在靶器官中的复制,从而使小鼠免于死亡。