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Pathogenicity of severe fever with thrombocytopenia syndrome virus in mice regulated in type I interferon signaling
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Park, Seok-Chan | - |
dc.contributor.author | Park, Jun Young | - |
dc.contributor.author | Choi, Jin Young | - |
dc.contributor.author | Lee, Sung-Geun | - |
dc.contributor.author | Eo, Seong Kug | - |
dc.contributor.author | Oem, Jae-Ku | - |
dc.contributor.author | Tark, Dong-Seob | - |
dc.contributor.author | You, Myungjo | - |
dc.contributor.author | Yu, Do-Hyeon | - |
dc.contributor.author | Chae, Joon-Seok | - |
dc.contributor.author | Kim, Bumseok | - |
dc.date.accessioned | 2021-01-07T06:59:25Z | - |
dc.date.available | 2021-01-07T16:00:24Z | - |
dc.date.issued | 2020-10-21 | - |
dc.identifier.citation | Laboratory Animal Research. 2020 Oct 21;36(1):38 | ko_KR |
dc.identifier.issn | 2233-7660 | - |
dc.identifier.uri | 10.1186/s42826-020-00070-0 | - |
dc.identifier.uri | https://hdl.handle.net/10371/171611 | - |
dc.description.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. | ko_KR |
dc.description.sponsorship | The research was supported by the Republic of Korea (Government-wide
R&D Fund project for infectious disease research (GFID), HG18C0084). | ko_KR |
dc.language.iso | en | ko_KR |
dc.publisher | BMC | ko_KR |
dc.subject | Severe fever with thrombocytopenia syndrome | - |
dc.subject | Type I interferon | - |
dc.subject | Mice | - |
dc.subject | Pathogenicity | - |
dc.title | Pathogenicity of severe fever with thrombocytopenia syndrome virus in mice regulated in type I interferon signaling | ko_KR |
dc.type | Article | ko_KR |
dc.contributor.AlternativeAuthor | 박찬석 | - |
dc.contributor.AlternativeAuthor | 박준영 | - |
dc.contributor.AlternativeAuthor | 최진영 | - |
dc.contributor.AlternativeAuthor | 이성근 | - |
dc.contributor.AlternativeAuthor | 어성국 | - |
dc.contributor.AlternativeAuthor | 엄재구 | - |
dc.contributor.AlternativeAuthor | 탁동섭 | - |
dc.contributor.AlternativeAuthor | 유명조 | - |
dc.contributor.AlternativeAuthor | 유도현 | - |
dc.contributor.AlternativeAuthor | 채준석 | - |
dc.contributor.AlternativeAuthor | 김범석 | - |
dc.citation.journaltitle | aboratory Animal Research | ko_KR |
dc.language.rfc3066 | en | - |
dc.rights.holder | The Author(s) | - |
dc.date.updated | 2020-10-25T04:19:22Z | - |
dc.citation.number | 1 | ko_KR |
dc.citation.startpage | 38 | ko_KR |
dc.citation.volume | 36 | ko_KR |
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