alpha-Defensin inhibits influenza virus replication by cell-mediated mechanism(s).

Journal Article (Journal Article)

The innate immune system mounts the first host response to pathogens. Because alpha-defensins, which are cationic antimicrobial peptides of polymorphonuclear neutrophils and other leukocytes, are important effectors of the innate immune system, we studied the antiviral activity of human alpha-defensin-1 (also known as "human neutrophil peptide-1" [HNP-1]) against influenza virus in vitro. Treatment of cell cultures with HNP-1 soon after infection resulted in marked inhibition of influenza virus replication and viral protein synthesis. This effect was not due to cytotoxicity or to a direct effect on the virus. Treatment of cells with HNP-1 followed by its removal before infection also inhibited viral replication, suggesting that the inhibition was due to the modulation of cellular pathways. HNP-1 treatment inhibited protein kinase C (PKC) activation in infected cells, suggesting the involvement of the PKC pathway. Our data expand the previously known activity of alpha -defensins against influenza virus. Characterizing the mechanism of action of alpha -defensins may lead to the identification of new strategies for prevention and therapy.

Full Text

Duke Authors

Cited Authors

  • Salvatore, M; Garcia-Sastre, A; Ruchala, P; Lehrer, RI; Chang, T; Klotman, ME

Published Date

  • September 15, 2007

Published In

Volume / Issue

  • 196 / 6

Start / End Page

  • 835 - 843

PubMed ID

  • 17703413

International Standard Serial Number (ISSN)

  • 0022-1899

Digital Object Identifier (DOI)

  • 10.1086/521027


  • eng

Conference Location

  • United States