Pathogenicity of severe fever with thrombocytopenia syndrome virus in mice regulated in type I interferon signaling
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Laboratory Animal Research
RESEARCH
Open Access
Pathogenicity of severe fever with thrombocytopenia syndrome virus in mice regulated in type I interferon signaling Severe fever with thrombocytopenia and type I interferon Seok-Chan Park1, Jun Young Park1,2, Jin Young Choi1, Sung-Geun Lee2, Seong Kug Eo1,2, Jae-Ku Oem1, Dong-Seob Tark2, Myungjo You1, Do-Hyeon Yu3, Joon-Seok Chae4 and Bumseok Kim1,2*
Abstract Severe fever with thrombocytopenia syndrome (SFTS) is an emerging zoonotic disease, which causes high fever, thrombocytopenia, and death in humans and animals in East Asian countries. The pathogenicity of SFTS virus (SFTS V) remains unclear. We intraperitoneally infected three groups of mice: wild-type (WT), mice treated with blocking anti-type I interferon (IFN)-α receptor antibody (IFNAR Ab), and IFNAR knockout (IFNAR−/−) mice, with four doses of SFTSV (KH1, 5 × 105 to 5 × 102 FAID50). The WT mice survived all SFTSV infective doses. The IFNAR Ab mice died within 7 days post-infection (dpi) with all doses of SFTSV except that the mice were infected with 5 × 102 FAID50 SFTSV. The IFNAR−/− mice died after infection with all doses of SFTSV within four dpi. No SFTSV infection caused hyperthermia in any mice, whereas all the dead mice showed hypothermia and weight loss. In the WT mice, SFTSV RNA was detected in the eyes, oral swabs, urine, and feces at 5 dpi. Similar patterns were observed in the IFNAR Ab and IFNAR−/− mice after 3 dpi, but not in feces. The IFNAR Ab mice showed viral shedding until 7 dpi. The SFTSV RNA loads were higher in organs of the IFNAR−/− mice compared to the other groups. Histopathologically, coagulation necrosis and mononuclear inflammatory cell infiltration in the liver and white pulp atrophy in the spleen were seen as the main lesions in the IFN signaling lacking mice. Immunohistochemically, SFTSV antigens were mainly detected in the marginal zone of the white pulp of the spleen in all groups of mice, but more viral antigens were observed in the spleen of the IFNAR−/− mice. Collectively, the IFN signaling-deficient mice were highly susceptible to SFTSV and more viral burden could be demonstrated in various excreta and organs of the mice when IFN signaling was inhibited. Keywords: Severe fever with thrombocytopenia syndrome, Type I interferon, Mice, Pathogenicity
* Correspondence: [email protected] 1 College of Veterinary Medicine, Jeonbuk National University, Iksan 54596, Republic of Korea 2 Korea Zoonosis Research Institute, Jeonbuk National University, Iksan 54531, Republic of Korea Full list of author information is available at the end of the article © The Author(s). 2020 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article
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