Lekstrom-Himes J A, LeBlanc R A, Pesnicak L, Godleski M, Straus S E
Medical Virology Section, Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
J Virol. 2000 Jul;74(14):6680-3. doi: 10.1128/jvi.74.14.6680-6683.2000.
Murine models of gamma interferon (IFN-gamma) deficiency demonstrate the role of this cytokine in attenuating acute herpes simplex virus (HSV) disease; however, the effect of IFN-gamma on the establishment and maintenance of neuronal latency and viral reactivation is not known. Using the IFN-gamma knockout (GKO) model of IFN-gamma deficiency and sensitive quantitative PCR methods, we show that IFN-gamma significantly reduces the ganglion content of latent HSV-1 in BALB/c mice, which in turn delays viral time to reactivation following UV irradiation. Similar effects were not seen in the C57BL/6 strain. These results indicate that IFN-gamma significantly attenuates latent HSV infection in the mouse model of ocular infection but has no impact on the maintenance of latency or virus reactivation.
γ干扰素(IFN-γ)缺乏的小鼠模型证明了这种细胞因子在减轻急性单纯疱疹病毒(HSV)疾病中的作用;然而,IFN-γ对神经元潜伏状态的建立和维持以及病毒再激活的影响尚不清楚。利用IFN-γ缺乏的IFN-γ基因敲除(GKO)模型和灵敏的定量PCR方法,我们发现IFN-γ显著降低了BALB/c小鼠潜伏HSV-1的神经节含量,这反过来又延迟了紫外线照射后病毒再激活的时间。在C57BL/6品系中未观察到类似的效果。这些结果表明,IFN-γ在眼部感染的小鼠模型中显著减轻潜伏HSV感染,但对潜伏状态的维持或病毒再激活没有影响。