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J Infect Dis. 2007 Sep 15;196(6):835-43. Epub 2007 Aug 10.

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

Author information

1
Division of Infectious Diseases, Mount Sinai School of Medicine, New York, NY 100129, USA. Mirella.Salvatore@mssm.edu

Abstract

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.

PMID:
17703413
DOI:
10.1086/521027
[Indexed for MEDLINE]

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