Kay M A, Manno C S, Ragni M V, Larson P J, Couto L B, McClelland A, Glader B, Chew A J, Tai S J, Herzog R W, Arruda V, Johnson F, Scallan C, Skarsgard E, Flake A W, High K A
Department of Pediatrics, Stanford University School of Medicine, Palo Alto, California, USA.
Nat Genet. 2000 Mar;24(3):257-61. doi: 10.1038/73464.
Pre-clinical studies in mice and haemophilic dogs have shown that introduction of an adeno-associated viral (AAV) vector encoding blood coagulation factor IX (FIX) into skeletal muscle results in sustained expression of F.IX at levels sufficient to correct the haemophilic phenotype. On the basis of these data and additional pre-clinical studies demonstrating an absence of vector-related toxicity, we initiated a clinical study of intramuscular injection of an AAV vector expressing human F.IX in adults with severe haemophilia B. The study has a dose-escalation design, and all patients have now been enrolled in the initial dose cohort (2 x 10(11) vg/kg). Assessment in the first three patients of safety and gene transfer and expression show no evidence of germline transmission of vector sequences or formation of inhibitory antibodies against F.IX. We found that the vector sequences are present in muscle by PCR and Southern-blot analyses of muscle biopsies and we demonstrated expression of F.IX by immunohistochemistry. We observed modest changes in clinical endpoints including circulating levels of F.IX and frequency of FIX protein infusion. The evidence of gene expression at low doses of vector suggests that dose calculations based on animal data may have overestimated the amount of vector required to achieve therapeutic levels in humans, and that the approach offers the possibility of converting severe haemophilia B to a milder form of the disease.
在小鼠和血友病犬身上进行的临床前研究表明,将编码凝血因子IX(FIX)的腺相关病毒(AAV)载体导入骨骼肌,可使FIX持续表达,其水平足以纠正血友病表型。基于这些数据以及其他表明不存在载体相关毒性的临床前研究,我们启动了一项针对重度B型血友病成年患者肌肉注射表达人FIX的AAV载体的临床研究。该研究采用剂量递增设计,目前所有患者均已纳入初始剂量队列(2×10¹¹vg/kg)。对首批三名患者进行的安全性、基因转移和表达评估显示,没有证据表明载体序列发生种系传播或形成针对FIX的抑制性抗体。通过对肌肉活检组织进行PCR和Southern印迹分析,我们发现肌肉中存在载体序列,并通过免疫组织化学证明了FIX的表达。我们观察到临床终点指标有适度变化,包括FIX的循环水平和FIX蛋白输注频率。低剂量载体的基因表达证据表明,基于动物数据进行的剂量计算可能高估了在人类中达到治疗水平所需的载体量,并且该方法有可能将重度B型血友病转变为病情较轻的形式。