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Wachinger, M. ; Kleinschmidt, A.* ; Winder, D.* ; von Pechmann, N. ; Ludvigsen, A. ; Neumann, M. ; Holle, R. ; Salmons, B.* ; Erfle, V. ; Brack-Werner, R.

Antimicrobial peptides melittin and cecropin inhibit replication of human immunodeficiency virus 1 by suppressing viral gene expression.

J. Gen. Virol. 79, 731-740 (1998)
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Antimicrobial peptides are effectors of innate immunity, providing their hosts with rapid non-specific defence against parasitic invaders. In this report, the effects are assessed of two well-characterized antimicrobial amphipathic peptides (melittin and cecropin) on human immunodeficiency virus 1 (HIV-1) replication and gene expression in acutely infected cells at subtoxic concentrations. Production of infectious, cell-free virus was inhibited in a dose-dependent manner, with ID50 values in the range 0.9-1.5 microM for melittin and 2-3 microM for cecropin. Analysis of the effect of melittin on cell-associated virus production revealed decreased levels of Gag antigen and HIV-1 mRNAs. Transient transfection assays with HIV long terminal repeat (LTR)-driven reporter gene plasmids indicated that melittin has a direct suppressive effect on activity of the HIV LTR. HIV LTR activity was also reduced in human cells stably transfected with retroviral expression plasmids for the melittin or cecropin gene. It is concluded that antimicrobial peptides such as melittin and cecropin are capable of inhibiting cell-associated production of HIV-1 by suppressing HIV-1 gene expression.
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Publication type Article: Journal article
Document type Scientific Article
Keywords LONG TERMINAL REPEAT; NF-KAPPA-B; HIV-1 LTR; ANTIBACTERIAL PEPTIDES; CHANNEL FORMATION; INNATE IMMUNITY; INSECT IMMUNITY; HUMAN-BRAIN; CELL-LINES; HTLV-III
Language english
Publication Year 1998
HGF-reported in Year 0
ISSN (print) / ISBN 0022-1317
e-ISSN 1465-2099
Quellenangaben Volume: 79, Issue: 4, Pages: 731-740 Article Number: , Supplement: ,
Publisher Society for General Microbiology
Reviewing status Peer reviewed
Institute(s) Institute of Virology (VIRO)
Department for Medical Information Systems (MEDIS)
Institute of Health Economics and Health Care Management (IGM)
PubMed ID 9568968
Erfassungsdatum 1998-12-31