Taylor J L, O'Brien W J
Invest Ophthalmol Vis Sci. 1985 Nov;26(11):1502-8.
The induction of interferon and the ability of interferon to induce the antiviral state were studied using rabbit corneal epithelial and stromal cells which were cultured for fewer than five passages. Interferon titers in the range of 7000 units/ml were induced in epithelial cell cultures and 76,000 units/ml in stromal cell cultures treated with UV-inactivated bluetongue virus. The interferon induced was stable to pH 2.0 treatment and heating to 56 degrees C for 16 hr. Infection of epithelial and stromal cell cultures with various strains of herpes simplex virus type 1 showed that all strains tested replicated to equivalent titers in the respective cell types, and that no detectable interferon was induced in stromal cells and only trace amounts in epithelial cells. Exogenously supplied rabbit interferon induced the antiviral state in cultures of both cell types restricting the replication of not only encephalomyocarditis virus but also herpes simplex virus. Sixty to ninety units of rabbit interferon reduced HSV-1 virus replication by 50%. Human interferons had less than 27% of the antiviral activity in rabbit cells than they had in a human cell line. The data indicate that exogenously supplied interferon may act to reduce the severity of herpetic keratitis by directly inducing the antiviral state in corneal epithelial and stromal cells. However, interferon endogenously produced by rabbit corneal cells in response to HSV-1 infection probably plays a minor role in the pathogenesis of ocular HSV-1 infections.
使用传代次数少于5次的兔角膜上皮细胞和基质细胞,研究了干扰素的诱导以及干扰素诱导抗病毒状态的能力。在用紫外线灭活的蓝舌病毒处理的上皮细胞培养物中诱导出的干扰素效价范围为7000单位/毫升,在基质细胞培养物中为76,000单位/毫升。所诱导的干扰素对pH 2.0处理和56℃加热16小时均稳定。用各种1型单纯疱疹病毒株感染上皮细胞和基质细胞培养物,结果显示所有测试菌株在各自的细胞类型中复制到相当的效价,并且在基质细胞中未诱导出可检测到的干扰素,在上皮细胞中仅诱导出微量干扰素。外源性提供的兔干扰素在两种细胞类型的培养物中诱导抗病毒状态,不仅限制脑心肌炎病毒的复制,也限制单纯疱疹病毒的复制。60至90单位的兔干扰素可使HSV-1病毒复制减少50%。人干扰素在兔细胞中的抗病毒活性比在人细胞系中的活性低27%。数据表明,外源性提供的干扰素可能通过直接诱导角膜上皮细胞和基质细胞中的抗病毒状态来减轻疱疹性角膜炎的严重程度。然而,兔角膜细胞对HSV-1感染内源性产生的干扰素可能在眼部HSV-1感染的发病机制中起次要作用。