McCarthy K, Tosolini F A
Lancet. 1975 Mar 22;1(7908):649-50. doi: 10.1016/s0140-6736(75)91756-0.
A new simian herpes virus with biological properties similar to herpes simplex and to simian "B" virus has been used as a model system for studying virus latency in dorsal root spinal sensory ganglia. Following intradermal injection, virus is present in the skin lesions and corresponding ganglia only, during the acute stage of the disease. By organ-culture techniques, latent virus was rescued from ganglia up to 2 years later. No latent virus was ever found in skin organ cultures of the primary site. Treatment with cortisone up to 18 months later reactivated virus latent in the ganglia, and virus returned to the skin where it produced small but typical herpes lesions which shed virus. Reactivation of Herpesvirus tamarinus was achieved after 28 months. This is believed to be the first report of a model system for the study of herpes latency in which skin lesions are found to recur, and provides an opportunity for more detailed investigations of the mechanisms of virus latency in man. The presumption that reactivation of skin lesions will also be possible in rhesus monkeys seropositive for "B" virus points to a possibly grave and largely unsuspected hazard for those engaged in primate research.
一种具有与单纯疱疹病毒和猿猴“B”病毒相似生物学特性的新型猿猴疱疹病毒已被用作研究背根脊髓感觉神经节中病毒潜伏状态的模型系统。皮内注射后，在疾病急性期，病毒仅存在于皮肤损伤处和相应的神经节中。通过器官培养技术，长达2年后仍能从神经节中拯救出潜伏病毒。在原发部位的皮肤器官培养物中从未发现潜伏病毒。长达18个月后用可的松治疗可重新激活潜伏在神经节中的病毒，病毒返回皮肤，在那里产生小的但典型的疱疹损伤并排出病毒。绢毛猴疱疹病毒在28个月后被重新激活。这被认为是关于研究疱疹潜伏状态的模型系统的首次报告，其中发现皮肤损伤会复发，并为更详细地研究人类病毒潜伏机制提供了机会。对于“B”病毒血清阳性的恒河猴，皮肤损伤也可能重新激活的推测表明，这对从事灵长类动物研究的人员来说可能是一个严重且很大程度上未被认识到的危险。
