Fernandez J A, Rodrigues E G, Tsuji M
Department of Medical and Molecular Parasitology, New York University School of Medicine, New York 10010, USA.
Viral Immunol. 2000;13(3):287-95. doi: 10.1089/08828240050144626.
In this article, we investigated the protective host immune mechanisms against acute murine cytomegalovirus (MCMV) infection. For this purpose, we used various knockout mice lacking molecules, which include interferon-gamma (IFN-gamma), interferon-gamma receptor (IFN-gamma-R), interferon regulatory factor-1 (IRF-1), inducible nitric oxide synthase (iNOS), and perforin. We also used mutant mice lacking Fas molecule. When we infected these mice with MCMV and determined the viral titers in their lungs at different time points, we found that IFN-gamma, IFN-gamma-R, IRF-1, iNOS, and perforin-deficient mice developed significantly higher titers of infectious MCMV in the lung, compared to those observed in their respective wild-type controls. In the lungs of Fas-mutant mice, viral titers were similar to those obtained in wild-type mice.
在本文中，我们研究了宿主针对急性小鼠巨细胞病毒（MCMV）感染的保护性免疫机制。为此，我们使用了多种缺乏特定分子的基因敲除小鼠，这些分子包括γ干扰素（IFN-γ）、γ干扰素受体（IFN-γ-R）、干扰素调节因子-1（IRF-1）、诱导型一氧化氮合酶（iNOS）和穿孔素。我们还使用了缺乏Fas分子的突变小鼠。当我们用MCMV感染这些小鼠并在不同时间点测定其肺部的病毒滴度时，我们发现，与各自的野生型对照相比，缺乏IFN-γ、IFN-γ-R、IRF-1、iNOS和穿孔素的小鼠肺部感染性MCMV的滴度显著更高。在Fas突变小鼠的肺部，病毒滴度与野生型小鼠相似。
