Sedmak D D, Chaiwiriyakul S, Knight D A, Waldmann W J
Department of Pathology, Ohio State University College of Medicine, Columbus, USA.
Arch Virol. 1995;140(1):111-26. doi: 10.1007/BF01309727.
Human cytomegalovirus (HCMV), a member of the virus family Herpesviridae that is associated with extensive worldwide morbidity and mortality in immunocompromised hosts, inhibits interferon-gamma (IFN gamma)-mediated induction of human leukocyte antigen (HLA) class II antigens on endothelial cells. In this study, the ability of HCMV-infected endothelial cells to synthesize interferon-beta (IFN beta), and the role of IFN beta in HCMV-mediated inhibition of HLA class II induction, was investigated. As determined by an encephalomyocarditis virus protection assay, HCMV-infected endothelial cell culture supernatants contained 240 IU/ml of IFN type I activity, of which 99.9% was IFN beta, as compared to the absence of IFN beta in mock-infected culture supernatants. UV-irradiated supernatants from HCMV-infected cultures inhibited induction of HLA class II in noninfected cultures by 24%. This inhibition could be abolished with 500 NU/ml of anti-IFN beta antibody. Addition of anti-IFN beta antibody directly to HCMV-infected cultures mitigated but did not abolish HLA class II antigen inhibition. Dual immunohistochemistry for HCMV and HLA DR demonstrated that infected cells, in contrast to noninfected cells, were rarely induced to express HLA class II even in the presence of anti-IFN beta antibody. These findings suggest that HCMV inhibits induction of HLA class II antigens by IFN beta dependent and independent mechanisms.
人巨细胞病毒(HCMV)是疱疹病毒科的成员,在免疫功能低下的宿主中与全球范围内广泛的发病率和死亡率相关,它可抑制干扰素-γ(IFNγ)介导的内皮细胞上人类白细胞抗原(HLA)II类抗原的诱导。在本研究中,研究了HCMV感染的内皮细胞合成干扰素-β(IFNβ)的能力,以及IFNβ在HCMV介导的HLA II类诱导抑制中的作用。通过脑心肌炎病毒保护试验测定,HCMV感染的内皮细胞培养上清液含有240 IU/ml的I型干扰素活性,其中99.9%是IFNβ,而 mock感染的培养上清液中不存在IFNβ。HCMV感染培养物的紫外线照射上清液可使未感染培养物中HLA II类的诱导降低24%。500 NU/ml的抗IFNβ抗体可消除这种抑制作用。将抗IFNβ抗体直接添加到HCMV感染的培养物中可减轻但不能消除HLA II类抗原的抑制作用。HCMV和HLA DR的双重免疫组织化学显示,与未感染细胞相比,即使在存在抗IFNβ抗体的情况下,感染细胞也很少被诱导表达HLA II类。这些发现表明,HCMV通过IFNβ依赖性和非依赖性机制抑制HLA II类抗原的诱导。