How does Cellular Heparan Sulfate Function in Viral Pathogenicity?  

作　　者：ZHU WuYang LI JiangJiao LIANG GuoDong 

机构地区：[1]Department of Viral Encephalitis, Institute for Viral Disease Control and Prevention, Chinese Center forDisease Control and Prevention and State Key Laboratory for Infectious Disease Prevention and Control(SKLID), Beijing 100052, China

出　　处：《Biomedical and Environmental Sciences》2011年第1期81-87,共7页生物医学与环境科学（英文版）

基　　金：supported by grants from the National Natural Science Foundation of China (No. 30970160);the Major Science and Technology Project for Infectious Disease (No. 2008ZX10004‐001; 2009ZX10004‐705);the Development Grant of the State Key Laboratory for Infectious Disease Prevention and Control (2008SKLID105)

摘　　要：Heparan sulfate （HS） is ubiquitously expressed on the surfaces and in the extracellular matrix of virtually all cell types, making it an ideal receptor for viral infection. Compared with wild‐type viruses, cell culture‐adapted laboratory strains exhibit more efficient binding to cellular HS receptors. HS‐binding viruses are typically cleared faster from the circulation and cause lower viremia than their non‐HS‐binding counterparts, suggesting that the HS‐binding phenotype is a tissue culture adaptation that lowers virus fitness in vivo. However, when inoculated intracranially, efficient cell attachment through HS binding can contribute to viral neurovirulence. The primary aim of this review is to discuss the roles of HS binding in viral pathogenicity, including peripheral virulence and neurovirulence. Understanding how heparan sulfate functions during virus infection in vivo may prove critical for elucidating the molecular mechanism of viral pathogenesis, and may contribute to the development of therapeutics targeting HS.Heparan sulfate （HS） is ubiquitously expressed on the surfaces and in the extracellular matrix of virtually all cell types, making it an ideal receptor for viral infection. Compared with wild‐type viruses, cell culture‐adapted laboratory strains exhibit more efficient binding to cellular HS receptors. HS‐binding viruses are typically cleared faster from the circulation and cause lower viremia than their non‐HS‐binding counterparts, suggesting that the HS‐binding phenotype is a tissue culture adaptation that lowers virus fitness in vivo. However, when inoculated intracranially, efficient cell attachment through HS binding can contribute to viral neurovirulence. The primary aim of this review is to discuss the roles of HS binding in viral pathogenicity, including peripheral virulence and neurovirulence. Understanding how heparan sulfate functions during virus infection in vivo may prove critical for elucidating the molecular mechanism of viral pathogenesis, and may contribute to the development of therapeutics targeting HS.

关 键 词：Heparan sulfate Viral pathogenicity RECEPTOR 

分 类 号：S852.659.6[农业科学—基础兽医学] S858.28[农业科学—兽医学]