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Pathogenicity of severe fever with thrombocytopenia syndrome virus in mice regulated in type I interferon signaling

Laboratory Animal Research 2020년 36권 1호 p.38 ~ 38
박석찬, 박준영, 최진영, 이성근, 어성국, 엄재구, 탁동섭, 유명조, 유도현, 채준석, 김범석,
소속 상세정보
박석찬 ( Park Seok-Chan ) - Chonbuk National University College of Veterinary Medicine
박준영 ( Park Jun-Young ) - Chonbuk National University College of Veterinary Medicine
최진영 ( Choi Jin-Young ) - Chonbuk National University College of Veterinary Medicine
이성근 ( Lee Sung-Geun ) - Chonbuk National University Korea Zoonosis Research Institute
어성국 ( Eo Seong-Kug ) - Chonbuk National University College of Veterinary Medicine
엄재구 ( Oem Jae-Ku ) - Chonbuk National University College of Veterinary Medicine
탁동섭 ( Tark Dong-Seob ) - Chonbuk National University Korea Zoonosis Research Institute
유명조 ( You Myung-Jo ) - Chonbuk National University College of Veterinary Medicine
유도현 ( Yu Do-Hyeon ) - Gyeongsang National University College of Veterinary Medicine
채준석 ( Chae Joon-Seok ) - Seoul National University College of Veterinary Medicine
김범석 ( Kim Bum-Seok ) - Chonbuk National University College of Veterinary Medicine

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 (SFTSV) 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.

키워드

Severe fever with thrombocytopenia syndrome; Type I interferon; Mice; Pathogenicity

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