Sidwell R W, Khare G P, Allen L B, Huffman J G, Witkowski J T, Simon L N, Robins R K
Chemotherapy. 1975;21(3-4):205-20. doi: 10.1159/000221861.
1-beta-D-ribofuranosyl-1,2,4-triazole-3-carboxamide (ribavirin) had significant in vitro activity against type 1 parainfluenza (Sendai) and type 3 parainogenic (HA-1) viruses. Activity was manifested as inhibition of both viral cytopathogenic effect and of recoverable virus or viral hemagglutinin titer. The minimum Sendai virus inhibitory concentration was determined to be approximately 3.2 mug/ml. Previous studies had determined the minimum concentration inhibiting HA-1 virus was approximately 1-10 mug/ml. The effect of time of addition of ribavirin to virus-infected cells was determined; maximal activity was seen when the drug added just prior to either virus or within 4-8 h after each virus, although anti-Senadi viral effects were still apparent when ribavirin was added as late as 24 h after the virus. Ribavirin had no effect on adsorption of HA-1 or Sendai virus to cells. Lethal Sendai virus infections of mice were significantly inhibited by multiple intraperitoneal ribavirin treatment, starting either 4 h before or up to 24 h after virus inoculation. Therapy starting 48, 72 or 96 h after virus exposure had a moderate degree of efficacy. Treatment using an aerosol chamber also was of moderate effectiveness, although the procedure was considered traumatic to the animals. A nonlethal, principally upper respiratory tract infection of hamsters induced by the HA-1 virus was inhibited by ribavirin therapy. Treatment administered intraperitoneally, per os or by aerosol chamber resulted in reduced 23-day antibody titers to the virus, presumably because of reduction of virus in the animal. In a separate experiment, intraperitoneal ribavirin therapy resulted in a 1 log10 or less reduction in virus titer in nasal washings from HA-1 virus-infected hamsters, whereas, when the drug was administered intranasally in a dry powder aerosol spray, nasal virus titers were reduced up to 2 log10 and a moderate virus-induced lung consolidation was completely inhibited.
1-β-D-呋喃核糖基-1,2,4-三唑-3-甲酰胺（利巴韦林）对1型副流感病毒（仙台病毒）和3型副流感病毒（HA-1）具有显著的体外活性。其活性表现为对病毒细胞病变效应以及可回收病毒或病毒血凝素滴度的抑制。测定仙台病毒的最小抑制浓度约为3.2μg/ml。先前的研究已确定抑制HA-1病毒的最小浓度约为1-10μg/ml。还测定了利巴韦林添加至病毒感染细胞的时间的影响；当在病毒感染前或每种病毒感染后4-8小时内添加药物时，可观察到最大活性，尽管在病毒感染后24小时添加利巴韦林时，抗仙台病毒的效果仍然明显。利巴韦林对HA-1或仙台病毒吸附至细胞没有影响。通过多次腹腔注射利巴韦林治疗，可显著抑制小鼠的致死性仙台病毒感染，治疗可在病毒接种前4小时或接种后24小时内开始。在病毒暴露后48、72或96小时开始治疗具有中等程度的疗效。使用气雾室进行治疗也具有中等效果，尽管该操作被认为对动物具有创伤性。利巴韦林治疗可抑制由HA-1病毒引起的仓鼠非致死性、主要为上呼吸道感染。通过腹腔内、经口或气雾室给药治疗可使针对该病毒的23天抗体滴度降低，这可能是由于动物体内病毒减少所致。在另一项实验中，腹腔注射利巴韦林治疗可使HA-1病毒感染的仓鼠鼻洗液中的病毒滴度降低1个对数10或更低，而当以干粉气雾剂喷雾形式经鼻给药时，鼻病毒滴度可降低高达2个对数10，并且可完全抑制中度的病毒诱导的肺实变。
