Suzuki Shunji, Carlos Maria P, Chuang Linda F, Torres José V, Doi Roy H, Chuang Ronald Y
Department of Medical Pharmacology and Toxicology, University of California, Davis, CA 95616, USA.
FEBS Lett. 2002 May 22;519(1-3):173-7. doi: 10.1016/s0014-5793(02)02746-1.
Methadone, a regimen for the treatment of opioid dependency, was found to induce the expression of CCR5, a co-receptor for human immunodeficiency virus (HIV)/simian form of HIV (SIV) entry, on human CEM x174 lymphocytes. Both CCR5 mRNA and protein were elevated in methadone-treated cells. A concomitant increase of mu opioid receptors was also observed. Upon methadone exposure, SIVmac239-infected CEM x174 cells released greater amounts of virus particles as revealed by both the number of syncytia formation and reverse transcriptase activities. Similar methadone effect was not observed on CEM x174 cells infected with other simian retroviruses that do not depend on CCR5 for cellular entry. These studies raise concerns considering methadone as an innocuous morphine substitute.
美沙酮是一种用于治疗阿片类药物依赖的疗法，研究发现它能在人CEM x174淋巴细胞上诱导趋化因子受体5（CCR5）的表达，CCR5是人类免疫缺陷病毒（HIV）/猿猴形式的HIV（SIV）进入细胞的共受体。在经美沙酮处理的细胞中，CCR5的信使核糖核酸（mRNA）和蛋白质水平均有所升高。同时还观察到μ阿片受体也有所增加。暴露于美沙酮后，如通过多核巨细胞形成数量和逆转录酶活性所显示的，感染了SIVmac239的CEM x174细胞释放出了更多的病毒颗粒。在感染了其他不依赖CCR5进入细胞的猿猴逆转录病毒的CEM x174细胞上未观察到类似的美沙酮效应。考虑到美沙酮是一种无害的吗啡替代品，这些研究引发了人们的担忧。
