Role of human beta defensin 3 during type I interferon mediated antiviral response against vesicular stomatitis virus
Mausumi Basu2, Srikanth Kota1, Amiya K Banerjee2, Santanu Bose1
1Department of Microbiology and Immunology, The University of Texas Health Science Center at San Antonio, San Antonio, TX, USA; 2Department of Molecular Genetics, Section of Virology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA
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 IFNstimulated 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.
Keywords: innate immunity, type I interferon, human beta defensin, virus infection
This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License. By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.Download Article [PDF]