Rausch D M, Heyes M P, Murray E A, Eiden L E
Section on Molecular Neuroscience, National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892, USA.
J Infect Dis. 1995 Jul;172(1):59-69. doi: 10.1093/infdis/172.1.59.
To assess the potential therapeutic effects of zidovudine, rhesus macaques were inoculated with simian immunodeficiency virus (SIV) strain SMM/B670 at birth and infused either continuously or intermittently with zidovudine for 6-7 months. Zidovudine did not prevent infection but did significantly increase survival time, which was associated with lower serum p26 viral core antigen levels, a lower virus burden in the cerebrospinal fluid (CSF), and lower CSF quinolinic acid levels than in untreated monkeys. Two of 5 infected, untreated monkeys developed motor impairment within 6 months following infection, whereas motor impairments did not occur in infected, zidovudine-treated monkeys until after the drug was discontinued. Zidovudine treatment was well tolerated by rhesus infants with minimal, transient side effects. These results demonstrate that zidovudine treatment significantly decreases virus load within the central nervous system (CNS) and delays the onset of CNS dysfunction and immune disease in rhesus monkeys perinatally infected with SIV.
为评估齐多夫定的潜在治疗效果，恒河猴在出生时接种猿猴免疫缺陷病毒（SIV）毒株SMM/B670，并连续或间歇输注齐多夫定6至7个月。齐多夫定虽不能预防感染，但显著延长了存活时间，这与血清p26病毒核心抗原水平较低、脑脊液（CSF）中病毒载量较低以及脑脊液喹啉酸水平低于未治疗的猴子有关。5只受感染的未治疗猴子中有2只在感染后6个月内出现运动障碍，而在受感染的经齐多夫定治疗的猴子中，直到停药后才出现运动障碍。恒河猴婴儿对齐多夫定治疗耐受性良好，副作用轻微且短暂。这些结果表明，齐多夫定治疗可显著降低围产期感染SIV的恒河猴中枢神经系统（CNS）内的病毒载量，并延迟CNS功能障碍和免疫疾病的发作。
