Antiviral activity of type I interferons and interleukins 29 and 28a (type III interferons) against Apeu virus |
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| Institution: | 1. Department of Pathological and Preventive Veterinary Science, The United Graduate School of Veterinary Science, Yamaguchi University, Yamaguchi, Japan;2. Institut de Recherche en Ecologie Tropicale (IRET), Centre National de Recherche Scientifique et Technologique (CENAREST), Libreville, Gabon;3. Transboundary Animal Diseases Research Centre, Joint Faculty of Veterinary Medicine, Kagoshima University, Kagoshima, Japan;4. Hakubi Center for Advanced Research, Kyoto University, Kyoto, Japan;5. Department of Virus Research, Institute for Frontier Life and Medical Sciences, Kyoto University, Kyoto, Japan;6. Department of Behavioral Physiology and Ecology, Joint Faculty of Veterinary Medicine, Kagoshima University, Kagoshima, Japan;7. Department of Biology, Faculty of Science, Toho University, Chiba, Japan;8. Kyoto University, Kyoto, Japan |
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| Abstract: | Interferons (IFNs) are cytokines with important immunomodulatory activity in vertebrates. Although type I IFNs and interleukins (IL) 29 and 28a (type III IFNs) bind to different cellular receptors and have distinct structures, most of their biological activities are redundant. Apeu virus (APEUV) is a member of the Bunyaviridae family isolated from the Brazilian rain forest. In this paper we evaluated the antiviral activity of type I and type III IFNs against APEUV. All tested IFNs were able to induce an antiviral state against the virus in a dose-dependent way. The activity of type III IFNs did not need the presence of type I IFNs. Mixing both types of IFNs did not improve the biological activity of each type alone. The tested IFNs were also able to protect human peripheral blood mononuclear cells from infection. IFN alpha2, IFN beta, IL-29 and IL-28a induced the expression of 2′,5′-oligoadenylate synthetase (2′5′OAS) and 6–16 genes. Although MxA gene was related to antiviral activity against Bunyaviruses, there was no induction of MxA in our model. We were able to show activity of type I and type III IFNs against a RNA virus, and that this activity is not dependent on MxA gene. |
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