Effect of interferon-alpha, interferon-gamma and tumour necrosis factor on African swine fever virus replication in porcine monocytes and macrophages.
Bovine interferon-alpha I1 (IFN-alpha I1) and porcine interferon-gamma (IFN-gamma) inhibited African swine fever virus replication in both porcine monocytes and alveolar macrophages. The most potent antiviral activity was observed with IFN-gamma-treated alveolar macrophages. The production of both a virulent (CC83) and a non-virulent (BA71) isolate of the virus was inhibited. Bovine tumour necrosis factor alpha did not show antiviral activity in either monocytes or alveolar macrophages. Rather, an increase of African swine fever virus production in tumour necrosis factor alpha-treated monocytes was found. An analysis of viral protein synthesis in IFN-alpha I1- and IFN-gamma-treated alveolar macrophages showed an inhibition of synthesis of some viral proteins. The inhibition of late proteins was very pronounced in IFN-gamma-treated cells, and it was probably a consequence of the inhibition of African swine fever virus DNA polymerase activity.
D000358:African Swine Fever Virus / Q000254:growth & development*; D000818:Animals; D004259:DNA-Directed DNA Polymerase / Q000378:metabolism; D007370:Interferon Type I / Q000494:pharmacology*; D007371:Interferon-gamma / Q000494:pharmacology*; D007497:Iridoviridae / Q000254:growth & development*; D007963:Leukocytes, Mononuclear / Q000382:microbiology; D008264:Macrophages / Q000382:microbiology; D011650:Pulmonary Alveoli / Q000166:cytology; D011994:Recombinant Proteins; D013552:Swine; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology*; D014764:Viral Proteins / Q000096:biosynthesis; D014779:Virus Replication
D007370:Interferon Type I; D011994:Recombinant Proteins; D014409:Tumor Necrosis Factor-alpha; D014764:Viral Proteins; D007371:Interferon-gamma; D004259:DNA-Directed DNA Polymerase