Streblow D N, Orloff S L, Nelson J A
Department of Molecular Microbiology and Immunology, Vaccine and Gene Therapy Institute, Oregon Health Sciences University, Portland, OR 97201, USA.
Curr Drug Targets Infect Disord. 2001 Aug;1(2):151-8. doi: 10.2174/1568005014606080.
The human cytomegalovirus (HCMV) has been implicated in the acceleration of vascular disease for some time. The development of vascular disease involves a chronic inflammatory process with many contributing factors, and of these, chemokines and their receptors have recently been identified as key mediators. Interestingly, HCMV encodes four potential chemokine receptors (US27, US28, UL33 and UL78). Of these virally-encoded chemokine receptors, US28 has been the most widely characterized. US28 binds many of the CC-chemokines, and this class of chemokines contributes to the development of vascular disease. Importantly, HCMV infection mediates in vitro SMC migration, which is dependent upon expression of US28 and CC-chemokine binding. US28 and the US28 functional homologues that are capable of inducing the migration of SMC represent potential targets in the treatment of CMV-accelerated vascular disease such as atherosclerosis, restenosis, and transplant vascular sclerosis.
一段时间以来,人类巨细胞病毒(HCMV)一直被认为与血管疾病的加速发展有关。血管疾病的发展涉及一个由多种因素促成的慢性炎症过程,其中,趋化因子及其受体最近被确定为关键介质。有趣的是,HCMV编码四种潜在的趋化因子受体(US27、US28、UL33和UL78)。在这些病毒编码的趋化因子受体中,US28的特征最为广泛。US28能结合多种CC趋化因子,而这类趋化因子会促进血管疾病的发展。重要的是,HCMV感染介导体外平滑肌细胞迁移,这依赖于US28的表达和CC趋化因子结合。US28以及能够诱导平滑肌细胞迁移的US28功能同源物是治疗CMV加速的血管疾病(如动脉粥样硬化、再狭窄和移植血管硬化)的潜在靶点。