Abstract |
In addition to their well-known antibacterial activity some antimicrobial peptides and proteins (AMPs) display also antiviral effects. A 27 aa peptide from the N-terminal part of human bactericidal/permeability-increasing protein (BPI) previously shown to harbour antibacterial activity inhibits the infectivity of multiple Influenza A virus strains (H1N1, H3N2 and H5N1) the causing agent of the Influenza pneumonia. In contrast, the homologous murine BPI-peptide did not show activity against Influenza A virus. In addition human BPI-peptide inhibits the activation of immune cells mediated by Influenza A virus. By changing the human BPI-peptide to the sequence of the mouse homologous peptide the antiviral activity was completely abolished. Furthermore, the human BPI-peptide also inhibited the pathogenicity of the Vesicular Stomatitis Virus but failed to interfere with HIV and measles virus. Electron microscopy indicate that the human BPI-peptide interferes with the virus envelope and at high concentrations was able to destroy the particles completely.
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Authors | Olaf Pinkenburg, Torben Meyer, Norbert Bannert, Steven Norley, Kathrin Bolte, Volker Czudai-Matwich, Susanne Herold, André Gessner, Markus Schnare |
Journal | PloS one
(PLoS One)
Vol. 11
Issue 6
Pg. e0156929
( 2016)
ISSN: 1932-6203 [Electronic] United States |
PMID | 27273104
(Publication Type: Journal Article)
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Chemical References |
- Antimicrobial Cationic Peptides
- Antiviral Agents
- Blood Proteins
- Peptide Fragments
- bactericidal permeability increasing protein
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Topics |
- Animals
- Antimicrobial Cationic Peptides
(metabolism, pharmacology)
- Antiviral Agents
(metabolism, pharmacology)
- Blood Proteins
(metabolism, pharmacology)
- Cells, Cultured
- Cricetinae
- Dogs
- Humans
- Influenza A Virus, H1N1 Subtype
(drug effects, pathogenicity)
- Influenza A Virus, H3N2 Subtype
(drug effects, pathogenicity)
- Influenza A Virus, H5N1 Subtype
(drug effects, pathogenicity)
- Influenza A virus
(drug effects, pathogenicity)
- Madin Darby Canine Kidney Cells
- Neutrophils
(metabolism)
- Peptide Fragments
(pharmacology)
- Virus Replication
(drug effects)
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