Vassão R, Pereira C A
Laboratório de Imunologia Viral, Instituto Butantan, SP, Brasil.
Braz J Med Biol Res. 1994 Oct;27(10):2407-11.
A/J mice became resistant to experimental MHV3 infection after immunization with UV-inactivated MHV3 (0% mortality, 0/10). Depletion of interferon (IFN) gamma-producing CD4+ T lymphocytes with monoclonal antibodies to CD4+ led to susceptibility to virus infection (60% of mortality, 6/10). The resistance to MHV3 infection of CD4+ T lymphocyte-depleted-A/J mice was restored by treatment with 1000 U of IFN gamma on days -1, 0, 1, 2, 3 and 4 (10% of mortality, 1/10). The low virus titers observed in resistant mice (controls or CD4+ depleted plus IFN gamma treated) were cleared 6 days after infection and the virus titers observed among susceptible mice (CD4+ depleted) increased gradually and peaked on day 6, when the animals died. Previous data, taken together with the direct evidence presented in this paper, provide strong evidence supporting the concept of an in vivo antiviral role of IFN gamma through a central action on the mechanisms of resistance to MHV3 infection.
用紫外线灭活的MHV3免疫后，A/J小鼠对实验性MHV3感染产生了抗性（死亡率为0%，10只中0只死亡）。用抗CD4 + 单克隆抗体清除产生干扰素（IFN）γ的CD4 + T淋巴细胞会导致对病毒感染敏感（死亡率为60%，10只中6只死亡）。在第-1、0、1、2、3和4天用1000 U的IFNγ治疗可恢复CD4 + T淋巴细胞耗竭的A/J小鼠对MHV3感染的抗性（死亡率为10%，10只中1只死亡）。在抗性小鼠（对照组或CD4 + 耗竭加IFNγ治疗组）中观察到的低病毒滴度在感染后6天清除，而在易感小鼠（CD4 + 耗竭组）中观察到的病毒滴度逐渐升高，并在第6天达到峰值，此时动物死亡。先前的数据与本文提供的直接证据一起，有力地支持了IFNγ通过对MHV3感染抗性机制的核心作用在体内发挥抗病毒作用这一概念。
