Role of human beta defensin 3 during type I interferon mediated antiviral response against vesicular stomatitis virus

Abstract

Type I interferons (IFN), IFN-α/β constitute a critical component of innate immunity against viruses. IFN-α/β activates JAK/STAT pathway resulting in expression of various IFN-stimulated antiviral proteins. While studying IFN-α/β signaling during virus infection, we identified human beta defensin-3 (HBD3) as an antiviral factor induced during IFN-α-mediated innate antiviral response in human lung epithelial cells. We showed that HBD3 is induced by IFN-α and purified HBD3 significantly inhibited vesicular stomatitis virus (VSV) infection. Further studies revealed that HBD3 confers its antiviral activity by blocking VSV cellular entry. An essential role of HBD3 during innate antiviral response was evident from loss of antiviral activity of IFN-α following HBD3 silencing by siRNA. Thus, we have identified HBD3 as an IFN-inducible antiviral factor that inhibits infection by blocking viral cellular entry. © 2010 Basu et al, publisher and licensee Dove Medical Press Ltd.