Blondeau J M, Aoki F Y, Glavin G B
Dept Medical Microbiology, University of Manitoba, Canada.
J Psychosom Res. 1993 Dec;37(8):843-9. doi: 10.1016/0022-3999(93)90173-d.
Clinical reports suggest that stress precipitates recurrent cutaneous Herpes simplex virus (HSV) infection, presumably by reactivating latent infection in sensory ganglia with subsequent centrifugal axonal spread to the skin. As an initial test of this hypothesis, rats with latent HSV, type-1, (HSV-1) infection in lumbar dorsal root ganglia (DRG) were exposed to a well-characterized acute stressor that produced gastric ulcers (U) and elevated plasma corticosterone (CS) concentrations. Stress-induced reactivation of latent HSV infection was suggested by the earlier appearance of cytopathic effect (CPE) in human foreskin fibroblast monolayers co-cultivated with ganglia from stressed rats than from nonstressed ones (4.5 +/- 0.2 and 6.4 +/- 0.4 [mean +/- SEM] days respectively; p < 0.001). No CPE was detected in monolayers co-cultivated with ganglia from non-infected rats. These initial results suggest that acute stress reactivates latent HSV-1 ganglionic infection.
临床报告表明，压力会促使复发性皮肤单纯疱疹病毒（HSV）感染，推测是通过激活感觉神经节中的潜伏感染，随后轴突离心性扩散至皮肤。作为对该假说的初步测试，将腰背部背根神经节（DRG）潜伏有1型单纯疱疹病毒（HSV-1）感染的大鼠暴露于一种特征明确的急性应激源下，该应激源会导致胃溃疡（U）并使血浆皮质酮（CS）浓度升高。与未受应激大鼠的神经节共同培养的人包皮成纤维细胞单层中，应激大鼠神经节的细胞病变效应（CPE）出现得更早，这提示潜伏HSV感染因应激而被激活（分别为4.5±0.2天和6.4±0.4天[平均值±标准误]；p<0.001）。与未感染大鼠的神经节共同培养的单层中未检测到CPE。这些初步结果表明，急性应激会激活潜伏的HSV-1神经节感染。
