Habu S, Akamatsu K, Tamaoki N, Okumura K
J Immunol. 1984 Nov;133(5):2743-7.
Susceptibility to infection with herpes simplex virus type 1 (HSV-1) was examined in euthymic as well as athymic nude mice which were continuously depleted of natural killer (NK) cell activity by i.v. injection of anti-asialo GM1. In those NK cell activity-depleted mice, the mortality rate of infection with HSV-1 and the virus titers in the brain, liver, and spleen were notably higher than in the control mice. The enhanced susceptibility was demonstrated only in the mice receiving anti-asialo GM1 and HSV-1 simultaneously, but not in the mice in which NK cell deletion was postponed by injecting the antisera 5 days after the virus inoculation. Interferon (IFN) production of peritoneal exudate cells was also reduced in the anti-asialo GM1-injected mice. The decline of resistance against HSV-1 infection proved to be primarily due to deletion of NK cells, but not due to the inability to produce IFN, because repeated injections of IFN increased the NK cell activity and prolonged the life of HSV-1-infected mice with an intact NK cell activity. In the NK cell activity-depleted mice, however, neither the NK cell activity nor the life span was improved by the administration of IFN.
在正常胸腺小鼠以及无胸腺裸鼠中检测了对1型单纯疱疹病毒（HSV-1）感染的易感性，这些小鼠通过静脉注射抗唾液酸GM1持续消耗自然杀伤（NK）细胞活性。在那些NK细胞活性被耗尽的小鼠中，HSV-1感染的死亡率以及脑、肝和脾中的病毒滴度显著高于对照小鼠。增强的易感性仅在同时接受抗唾液酸GM1和HSV-1的小鼠中表现出来，而在病毒接种5天后注射抗血清从而使NK细胞缺失延迟的小鼠中未观察到。注射抗唾液酸GM1的小鼠腹腔渗出细胞的干扰素（IFN）产生也减少。事实证明，对HSV-1感染抵抗力的下降主要是由于NK细胞的缺失，而非无法产生IFN，因为反复注射IFN可增加NK细胞活性并延长具有完整NK细胞活性的HSV-1感染小鼠的寿命。然而，在NK细胞活性被耗尽的小鼠中，给予IFN既不能提高NK细胞活性，也不能延长其寿命。
