Interferon-gamma enhances resolution of herpes simplex virus type 2 infection of the murine genital tract

Interferon-gamma enhances resolution of herpes simplex virus type 2 infection of the murine genital tract
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DOI:
10.1006/viro.1997.8441
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发表时间:
1997-03-03
期刊:
影响因子:
3.7
通讯作者:
Bernstein, DI
Bernstein, DI
中科院分区:
医学3区
文献类型:
--
作者:
Milligan, GN;Bernstein, DI

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干扰素-γ(IFN γ)在解决HSV-2阴道感染和阴道粘膜中这种细胞因子的细胞来源的要求进行了评估。阴道分泌物中的IFN γ水平在HSV-2接种后第2天和第5天达到峰值。自然杀伤细胞(NK)细胞耗竭大大减少了IFN γ的早期产生,但对病毒清除率没有显着影响。CD 4(+)T细胞主要负责IFN γ水平的第二个峰值,并且在病毒接种后3天开始中和该IFN γ延迟但不阻止病毒从阴道清除。HSV-2在CD 4(+)和CD 8(+)T细胞耗竭的小鼠中持续存在,而在CD 4(+)T细胞耗竭的小鼠中清除延迟,但在CD 8(+)T细胞耗竭的小鼠中不存在,这证明了T细胞依赖性和CD 4(+)T细胞在感染消退中的主要作用。总之,这些数据表明,IFN γ不是病毒清除所必需的,但在增强T细胞介导的清除机制中起重要作用。这些结果的含义是,在生殖道局部产生的IFN γ增强了病毒清除,并可能最终是重要的,以减少感染感觉神经节的病毒量。(C)北京:科学出版社.
The requirement for interferon-gamma (IFN gamma) in resolution of an HSV-2 vaginal infection and the cellular sources of this cytokine in the vaginal mucosa were assessed. IFN gamma levels in vaginal secretions peaked on Days 2 and 5 following HSV-2 inoculation. Natural killer (NK) call depletion greatly diminished the early production of IFN gamma but had no significant effect on the rate of virus clearance. CD4(+) T cells were primarily responsible for the second peak of IFN gamma levels and neutralization of this IFN gamma beginning 3 days after virus inoculation delayed, but did not prevent, virus clearance from the vagina. HSV-2 persisted in mice depleted of both CD4(+) and CD8(+) T cells while clearance was delayed in CD4(+), but not CD8(+) T cell-depleted mice, demonstrating the T cell dependence and predominant role of CD4(+) T cells in resolution of the infection. Together, these data suggest that IFN gamma is not essential for virus clearance but plays an important role in enhancing T cell-mediated clearance mechanisms. The implication of these results is that IFN gamma produced locally in the genital tract enhances virus clearance and may ultimately be important for reducing the amount of virus available to infect sensory ganglia. (C) 1997 Academic Press.