Role of trehalose dimycolate-induced interferon-α/β in the restriction of encephalomyocarditis virus growth in vivo and in peritoneal macrophage cultures
Autor: | C. Labarre, A.M. Quero, J.F. Petit, E. Guillemard, G. Lemaire, R. Kergot, M. Geniteau-Legendre |
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Rok vydání: | 1995 |
Předmět: |
medicine.medical_treatment
Alpha interferon Biology Antiviral Agents Virus Cell Line Microbiology Mice chemistry.chemical_compound In vivo Virology Cardiovirus Infections medicine Animals Ascitic Fluid Macrophage Encephalomyocarditis virus Cells Cultured Interferon alfa Pharmacology Interferon-alpha Interferon-beta Trehalose dimycolate Disease Models Animal Cytokine chemistry Cell culture Macrophages Peritoneal Cord Factors Female medicine.drug |
Zdroj: | Antiviral Research. 28:175-189 |
ISSN: | 0166-3542 |
DOI: | 10.1016/0166-3542(95)00047-p |
Popis: | Preventive intraperitoneal trehalose dimycolate (TDM) treatment of mice, inoculated with encephalomyocarditis (EMC) virus by the same route, caused restriction of virus growth in the peritoneum, which was correlated to IFN production in peritoneal fluids prior to infection. Peritoneal macrophages from TDM-treated mice (TDM-PM) spontaneously secreted IFN-alpha/beta in large amounts. By their supernatants, TDM-PM could transfer an antiviral state against EMC virus to permissive resident peritoneal macrophages from control mice. IFN-alpha/beta produced by TDM-PM was found to be involved in this transfer activity. TDM-PM also exerted a strong antiviral effect on EMC virus-infected L-929 cells, which increased with time and the macrophage-target cell ratio. This activity also occurred by an IFN-alpha/beta-dependent mechanism. These data point to the role of IFN-alpha/beta production prior to EMC virus infection in the antiviral activities of TDM-PM and, more generally, in the outcome of viral infection. |
Databáze: | OpenAIRE |
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