期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：1998
卷号：95
期号：12
页码：7074-7079
DOI：10.1073/pnas.95.12.7074
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：Newly emerged hantaviruses replicate primarily in the pulmonary endothelium, cause acute platelet loss, and result in hantavirus pulmonary syndrome (HPS). We now report that specific integrins expressed on platelets and endothelial cells permit the cellular entry of HPS-associated hantaviruses. Infection with HPS-associated hantaviruses, NY-1 and Sin Nombre virus (SNV), is inhibited by antibodies to {beta}3 integrins and by the {beta}3-integrin ligand, vitronectin. In contrast, infection with the nonpathogenic (no associated human disease) Prospect Hill virus was inhibited by fibronectin and {beta}1-specific antibodies but not by {beta}3-specific antibodies or vitronectin. Transfection with recombinant IIb{beta}3 or v{beta}3 integrins rendered cells permissive to NY-1 and SNV but not Prospect Hill virus infection, indicating that IIb{beta}3 and v{beta}3 integrins mediate the entry of NY-1 and SNV hantaviruses. Furthermore, entry is divalent cation independent, not blocked by arginine-glycine-aspartic acid peptides and still mediated by, ligand-binding defective, IIb{beta}3-integrin mutants. Hence, NY-1 and SNV entry is independent of {beta}3 integrin binding to physiologic ligands. These findings implicate integrins as cellular receptors for hantaviruses and indicate that hantavirus pathogenicity correlates with integrin usage.
