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
Language
- eng
Conference Location
- United States