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ORIGINAL RESEARCH article

Front. Microbiol.
Sec. Virology
Volume 15 - 2024 | doi: 10.3389/fmicb.2024.1452739

Limitations of a Proper SFTSV Mouse Model Using Human Ctype Lectin Receptors

Provisionally accepted
You Min Kim You Min Kim 1Hyo-Jin Ro Hyo-Jin Ro 2,3Jae Hoon Lee Jae Hoon Lee 1,4*Yaechan Song Yaechan Song 1*Han-Woong Lee Han-Woong Lee 1,4*Nam-Hyuk Cho Nam-Hyuk Cho 2,3,5,6*
  • 1 Department of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul, Seoul, Republic of Korea
  • 2 Department of Biomedical Sciences, College of Medicine, Seoul National University, Seoul, Republic of Korea
  • 3 Department of Microbiology, College of Medicine, Seoul National University, Seoul, Seoul, Republic of Korea
  • 4 GEMCRO, Inc, Seoul, Republic of Korea
  • 5 Institute of Endemic Diseases, Medical Research Center, Seoul National University, Seoul, Republic of Korea
  • 6 Seoul National University Bundang Hospital, Seongnam-si, Gyeonggi, Republic of Korea

The final, formatted version of the article will be published soon.

    Severe Fever with Thrombocytopenia Syndrome Virus (SFTSV) is a tick-borne virus with a human mortality rate of up to 30%, posing a significant threat to public health. However, the lack of suitable research models has impeded the development of effective human vaccines. In this study, we engineered transgenic mice (3xTg) using a novel construct that simultaneously expresses three C-type Lectin receptors, identified as critical SFTSV entry receptors. While this construct substantially enhanced viral binding and infection in BJAB cells, the 3xTg mice exhibited only limited SFTSV replication in the lymph nodes and spleen, without significant impacts on morbidity or mortality. These findings highlight that the overexpression of entry receptors alone is insufficient to fully recapitulate human SFTSV infection in mice. Moreover, our results reveal that the introduction of multiple entry receptors does not necessarily translate to enhanced infection efficacy. This underscores the need for further investigation into the interplay between SFTSV entry mechanisms and host factors to develop more robust mouse models. Advancing such models will be crucial for unraveling the pathogenesis of SFTS pathology and improving strategies for its prevention and treatment in humans.

    Keywords: Severe fever thrombocytopenia syndrome virus, DC-SIGN, DC-SIGNR, LSECtin, Transgenic mice

    Received: 21 Jun 2024; Accepted: 04 Dec 2024.

    Copyright: © 2024 Kim, Ro, Lee, Song, Lee and Cho. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence:
    Jae Hoon Lee, Department of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul, 03722, Seoul, Republic of Korea
    Yaechan Song, Department of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul, 03722, Seoul, Republic of Korea
    Han-Woong Lee, Department of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul, 03722, Seoul, Republic of Korea
    Nam-Hyuk Cho, Department of Biomedical Sciences, College of Medicine, Seoul National University, Seoul, 110-799, Republic of Korea

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