Mikerov Anatoly N, White Mitch, Hartshorn Kevan, Wang Guirong, Floros Joanna
Department of Cellular and Molecular Physiology, H166, The Pennsylvania State University College of Medicine, 500 University Drive, Hershey, PA 17033, USA.
Med Microbiol Immunol. 2008 Mar;197(1):9-12. doi: 10.1007/s00430-007-0051-4. Epub 2007 May 23.
Surfactant protein A (SP-A) inhibits hemagglutination (HA) activity and infectivity of influenza A viruses (IAV). As we have showed before in different assays, SP-A2 gene products are more active than SP-A1. Here, we hypothesized that SP-A1 and SP-A2 mammalian CHO-cell-expressed proteins also differentially modulate HA inhibition of IAV. We found that both SP-A1 and SP-A2 equally displayed alpha(2,3)-linked sialic acids, and had similar activity against a strain (PR-8) that preferentially binds to alpha(2,3)-linked sialic acids. Based on these findings, we speculate that in human lung SP-A1 and SP-A2 will not be different in their activity against IAV that preferably bind to alpha(2,3)-linked sialic acids (like avian strains).
表面活性蛋白A(SP-A)可抑制甲型流感病毒(IAV)的血凝(HA)活性和感染性。正如我们之前在不同实验中所表明的,SP-A2基因产物比SP-A1更具活性。在此,我们推测哺乳动物CHO细胞表达的SP-A1和SP-A2蛋白在调节IAV的HA抑制方面也存在差异。我们发现SP-A1和SP-A2均同样展示出α(2,3)连接的唾液酸,并且对优先结合α(2,3)连接唾液酸的毒株(PR-8)具有相似的活性。基于这些发现,我们推测在人类肺部,SP-A1和SP-A2对优先结合α(2,3)连接唾液酸的IAV(如禽源毒株)的活性不会有所不同。