Haisma Hidde J, Boesjes Marije, Beerens Antoine M, van der Strate Barry W A, Curiel David T, Plüddemann Annette, Gordon Siamon, Bellu Anna Rita
Department of Therapeutic Gene Modulation, Groningen University Institute for Drug Exploration, University of Groningen, The Netherlands.
Mol Pharm. 2009 Mar-Apr;6(2):366-74. doi: 10.1021/mp8000974.
Adenoviruses are common pathogens associated with respiratory diseases, gastrointestinal illnesses and/or conjunctivitis. Currently, this virus is used as a vector in gene therapy trials. The promise of viral gene therapy applications is substantially reduced because the virus is cleared by liver macrophages upon systemic administration. The mechanism underlying adenoviral tropism to and degradation in macrophages is poorly understood. We identified a new adenoviral receptor, the scavenger receptor A (SR-A), responsible for uptake of the virus in macrophages. CHO cells expressing SR-A showed increased viral transgene expression when compared with wild type cells. Preincubation of J774 macrophage cells with SR-A ligands decreased significantly adenoviral uptake. Electron-microscopy analysis of infected J774 cells showed activation of a viral degradation pathway. Infection of mice with adenovirus resulted in a substantial decrease of the virus in liver macrophages when SR-A was blocked. Our data provide a basis for understanding of the adenoviral uptake and degradation mechanism in macrophages in vitro and in vivo. Inhibition of adenoviral SR-A uptake can be utilized in gene therapy applications to increase its efficiency and efficacy.
腺病毒是与呼吸道疾病、胃肠道疾病和/或结膜炎相关的常见病原体。目前,这种病毒在基因治疗试验中用作载体。由于全身给药后病毒会被肝脏巨噬细胞清除,病毒基因治疗应用的前景大打折扣。腺病毒在巨噬细胞中的嗜性和降解的潜在机制尚不清楚。我们鉴定出一种新的腺病毒受体,即清道夫受体A(SR-A),它负责巨噬细胞对病毒的摄取。与野生型细胞相比,表达SR-A的CHO细胞显示出病毒转基因表达增加。用SR-A配体对J774巨噬细胞进行预孵育可显著降低腺病毒摄取。对受感染的J774细胞进行电子显微镜分析显示了病毒降解途径的激活。当SR-A被阻断时,用腺病毒感染小鼠会导致肝脏巨噬细胞中病毒大量减少。我们的数据为理解体外和体内巨噬细胞中腺病毒的摄取和降解机制提供了基础。抑制腺病毒SR-A摄取可用于基因治疗应用,以提高其效率和疗效。