Bruning J H, Persoons M, Lemström K, Stals F S, De Clercq E, Bruggeman C A
Department of Medical Microbiology, University of Limburg, Maastricht, The Netherlands.
Transpl Int. 1994;7 Suppl 1:S365-70. doi: 10.1111/j.1432-2277.1994.tb01393.x.
Effects of acute cytomegalovirus (CMV) infections on transplantation-associated atherosclerosis (TxAA) were studied in a rat model for chronic vascular rejection. Rats underwent orthotopic abdominal allogeneic aorta transplantation. Neo-intima formation and media thinning was quantitated by measurement of cross-sectional surface areas (CSA) at day 50 post transplantation (Tx). Acute rat cytomegalovirus (RCMV) infection, established at the moment of maximum intimal proliferation and influx of inflammatory cells in the adventitia, resulted in enhanced neo-intima formation, accompanied by increased influx and proliferation of smooth muscle cells (smc) in the intima. This effect was completely inhibited by HPMPC, a very potent and selective inhibitor of CMV replication, indicating the virus specificity of the measured effects. Despite increased neointima formation, media thinning ("necrosis") was not affected by RCMV infection.
在慢性血管排斥反应的大鼠模型中研究了急性巨细胞病毒（CMV）感染对移植相关动脉粥样硬化（TxAA）的影响。大鼠接受原位腹部同种异体主动脉移植。通过测量移植后（Tx）第50天的横截面积（CSA）对新生内膜形成和中膜变薄进行定量。在最大内膜增殖和外膜炎症细胞流入时建立急性大鼠巨细胞病毒（RCMV）感染，导致新生内膜形成增强，同时内膜中平滑肌细胞（SMC）的流入和增殖增加。这种作用被CMV复制的一种非常有效且选择性的抑制剂HPMPC完全抑制，表明所测效应具有病毒特异性。尽管新生内膜形成增加，但RCMV感染并未影响中膜变薄（“坏死”）。
