Monoclonal antibodies. Administrati

Monoclonal antibodies. Administration of rabies virus–neutralizing monoclonal antibodies (e.g., monoclonal antibody 1112-1) has been shown to clear rabies virus infection from the CNS in a rodent model when administered before the onset of clinical signs, resulting in the survival of experimentally infected rats [23]. This suggests that therapy with ⩾1 monoclonal antibodies may prove to be effective therapeutically in the future. Human monoclonal antibodies or humanized mouse monoclonal antibodies would be preferable to mouse monoclonal antibodies. Evaluation of this strategy would require development of an investigational drug protocol.
Ribavirin. Ribavirin (1-β-D-Ribofuranosyl-1H-1,2,4-triazole-3-carboxamide) is a broad-spectrum antiviral agent with many intrinsic mechanisms that can influence its overall antiviral properties [19]. Ribavirin is a purine analogue and an RNA mutagen that induces mutations by acting as a template for incorporation of cytidine and uridine with equal efficiency [24]. Ribavirin also has immunomodulatory properties that may, in part, account for its antiviral properties in vivo [25]. Ribavirin has in vitro activity against rabies virus infection [26, 27], although efficacy was not demonstrated in a study that used animal models [28]. Ribavirin is typically administered intravenously with both loading and maintenance doses. There is limited information about its penetration across the intact blood-brain barrier, which may be marginal, because rapid uptake into CSF was not observed in rats and rhesus monkeys [29]. However, significant levels of ribavirin were observed in CSF after orally administered ribavirin therapy was given for several weeks to patients with AIDS and AIDS-related complex [30]. Intraventricular administration of ribavirin via an Ommaya reservoir, in addition to therapy by the intravenous route, would be a therapeutic option at the present time. One patient with rabies who was treated with a combination of intrathecal and intravenous ribavirin therapy demonstrated no apparent benefit [16].

結果 (中文) 1:

单克隆抗体。狂犬病病毒 — — 压制单克隆抗体的管理 (例如，单克隆抗体 1112年-1） 已被证明清除狂犬病病毒感染从中枢神经系统中啮齿动物模型时管理之前发病的临床症状，从而导致的生存实验感染大鼠 [23]。这表明，⩾1 单克隆抗体治疗可能证明是有效治疗的未来。人类单克隆抗体或人性化的鼠单克隆抗体可取到鼠标单克隆抗体。这一战略的评价需要发展的一种试验药物协议。三氮唑核苷。三氮唑核苷 (1-β-D-Ribofuranosyl-1H-1,2,4-triazole-3-carboxamide) 是广谱的抗病毒剂与许多内在的机制可以影响其整体抗病毒性能 [19]。三氮唑核苷是一种嘌呤类似物和 RNA 诱变剂诱发基因突变作为纳入胞苷、 尿苷的模板与公平效率 [24]。利巴韦林也有可能，部分，占体内 [25] 及其抗病毒性能的免疫调节特性。利巴韦林有体外活性抗狂犬病病毒感染 [26，27]，虽然效果不显示在研究中使用动物模型 [28]。利巴韦林，通常是与加载和维护剂量静脉注射。有是有限的信息及其渗透整个完整血-脑屏障的这可能是边际，因为快速吸收入脑脊液不被观察了大鼠和恒河猴 [29]。然而，显著水平的利巴韦林观察脑脊液后口服利巴韦林治疗给出了几个星期到患者艾滋病和艾滋病-相关复杂 [30]。利巴韦林通过 Ommaya 水库，除了通过静脉途径治疗脑室管理工作会在目前的治疗选择。鞘内注射和静脉注射利巴韦林治疗结合治疗狂犬病一患者表现出没有明显的好处 [16]。

結果 (中文) 3:

单克隆抗体。狂犬病毒中和性单克隆抗体–管理（例如，单克隆抗体1112-1）已经显示出明确的狂犬病毒感染的动物模型中的中枢给药时出现临床症状之前，导致在实验感染大鼠[ 23 ]生存。这表明，⩾1单克隆抗体治疗可能是未来治疗有效。人单克隆抗体或人源化的小鼠单克隆抗体比鼠单克隆抗体更可取。这一战略的评价需要研究药物协议开发。Ribavirin。Ribavirin（1—β- d-ribofuranosyl-1h-1,2,4-triazole-3-carboxamide）是一种具有许多内在的机制，会影响其整体的抗病毒特性[ 19 ]广谱抗病毒药物。Ribavirin是一个嘌呤类似物和RNA诱变剂诱发突变的作用对于胞苷、尿苷掺入效率与平等[ 24 ]一个模板。Ribavirin还具有免疫调节特性的可能，部分，其在体内的抗病毒性能[ 25 ]。Ribavirin在体外对狂犬病毒感染[ 26，27 ]，虽然效果不是在研究中使用的动物模型证明[ 28 ]。Ribavirin是典型的静脉注射用的装载和维持剂量。有有限的信息，它的渗透在完整的血脑屏障，这可能是微不足道的，因为快速吸收到脑脊液中没有观察到大鼠和恒河猴[ 29 ]。然而，利巴韦林显著水平后口服利巴韦林治疗了几个星期与艾滋病和艾滋病相关的复杂的[ 30 ]患者CSF中观察。通过Ommaya储液囊利巴韦林脑室内注射治疗，除了通过静脉途径，将目前的治疗选择。一例狂犬病谁结合鞘内注射和静脉注射利巴韦林治疗没有表现出明显的利益[ 16 ]处理。