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Jeong, Haengdueng; Woo Lee, Youn; Park, In Ho; Noh, Hyuna; Kim, Sung-Hee; Kim, Jiseon; Jeon, Donghun; Jang, Hui Jeong; Oh, Jooyeon; On, Dain; Uhm, Chanyang; Cho, Kyungrae; Oh, Heeju; Yoon, Suhyeon; Seo, Jung Seon; Kim, Jeong Jin; Seok, Sang-Hyuk; Lee, Yu Jin; Hong, Seung-Min; An, Se-Hee; Yeon Kim, Seo; Kim, Young Been; Hwang, Ji-Yeon; Lee, Hyo-Jung; Kim, Hong Bin; Jeong, Dae Gwin; Song, Daesub; Song, Manki; Park, Man-Seong; Choi, Kang-Seuk; Park, Jun Won; Seo, Jun-Young; Yun, Jun-Won; Shin, Jeon-Soo; Lee, Ho-Young; Nam, Ki Taek; Seong, Je Kyung
Disease models & mechanisms, 11/2022, Letnik: 15, Številka: 11Journal Article
ABSTRACT Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the etiological agent of COVID-19, causes life-threatening disease. This novel coronavirus enters host cells via the respiratory tract, promoting the formation of severe pulmonary lesions and systemic disease. Few animal models can simulate the clinical signs and pathology of COVID-19 patients. Diverse preclinical studies using K18-hACE2 mice and Syrian golden hamsters, which are highly permissive to SARS-CoV-2 in the respiratory tract, are emerging; however, the systemic pathogenesis and cellular tropism of these models remain obscure. We intranasally infected K18-hACE2 mice and Syrian golden hamsters with SARS-CoV-2, and compared the clinical features, pathogenesis, cellular tropism and infiltrated immune-cell subsets. In K18-hACE2 mice, SARS-CoV-2 persistently replicated in alveolar cells and caused pulmonary and extrapulmonary disease, resulting in fatal outcomes. Conversely, in Syrian golden hamsters, transient SARS-CoV-2 infection in bronchial cells caused reversible pulmonary disease, without mortality. Our findings provide comprehensive insights into the pathogenic spectrum of COVID-19 using preclinical models.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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Povezave do osebnih bibliografij avtorjev | Povezave do podatkov o raziskovalcih v sistemu SICRIS |
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Vir: Osebne bibliografije
in: SICRIS
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