Comparisonof the pathogenesis of SARS-CoV-2 infection inK18-hACE2 miceand Syrian golden hamstermodels

Haengdueng Jeong; Youn Woo Lee; In Ho Park; Hyuna Noh; Sung Hee Kim; Jiseon Kim; Donghun Jeon; Hui Jeong Jang; Jooyeon Oh; Dain On; Chanyang Uhm; Kyungrae Cho; Heeju Oh; Suhyeon Yoon; Jung Seon Seo; Jeong Jin Kim; Sang Hyuk Seok; Yu Jin Lee; Seung Min Hong; Se Hee An; Seo Yeon Kim; Young Been Kim; Ji Yeon Hwang; Hyo Jung Lee; Hong Bin Kim; Dae Gwin Jeong; Daesub Song; Manki Song; Man Seong Park; Kang Seuk Choi; Jun Won Park; Jun Young Seo; Jun Won Yun; Jeon Soo Shin; Ho Young Lee; Ki Taek Nam; Je Kyung Seong

doi:10.1242/dmm.049632

Comparisonof the pathogenesis of SARS-CoV-2 infection inK18-hACE2 miceand Syrian golden hamstermodels

Haengdueng Jeong, Youn Woo Lee, In Ho Park, Hyuna Noh, Sung Hee Kim, Jiseon Kim, Donghun Jeon, Hui Jeong Jang, Jooyeon Oh, Dain On, Chanyang Uhm, Kyungrae Cho, Heeju Oh, Suhyeon Yoon, Jung Seon Seo, Jeong Jin Kim, Sang Hyuk Seok, Yu Jin Lee, Seung Min Hong, Se Hee AnSeo Yeon Kim, Young Been Kim, Ji Yeon Hwang, Hyo Jung Lee, Hong Bin Kim, Dae Gwin Jeong, Daesub Song, Manki Song, Man Seong Park, Kang Seuk Choi, Jun Won Park, Jun Young Seo, Jun Won Yun, Jeon Soo Shin, Ho Young Lee, Ki Taek Nam, Je Kyung Seong

BioMedical Science Institute

Research output: Contribution to journal › Article › peer-review

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Abstract

SARS-CoV-2, the etiological agentofCOVID-19, causeslife-threatening disease. This novel coronavirusenters host cellsvia the respiratory tract,promoting the formation ofsevere pulmonary lesions andsystemic disease. Few animal models can simulate the clinical signs and pathology ofCOVID-19patients.Diverse preclinical studies using K18-hACE2 mice and Syrian golden hamsters, which are highly permissive toSARS-CoV-2 in therespiratory tract, are emerging; however, the systemic pathogenesis and cellular tropism of these models remain obscure. We intranasally infected K18-hACE2 mice and Syrian golden hamsterswith SARS-CoV-2, and compared the clinical features, pathogenesis, cellular tropism,and infiltrated immune-cellsubsets. In K18-hACE2 mice, SARS-CoV-2 persistently replicated inalveolar cells and causedpulmonary and extra-pulmonary disease, resulting in fataloutcomes. Conversely, in Syrian golden hamsters, transient SARS-CoV-2infectioninbronchial cells causedreversible pulmonary disease,without mortality. Our findings provide comprehensive insightsinto thepathogenic spectrum of COVID-19 using pre-clinical models.

Original language	English
Journal	DMM Disease Models and Mechanisms
Volume	15
Issue number	11
DOIs	https://doi.org/10.1242/dmm.049632
Publication status	Published - 2022 Nov

Bibliographical note

Funding Information:
Funding: This project was supported by the Korea Mouse Phenotyping Project (NRF-2016M3A9D5A01952416) and by the Brain Korea 21 PLUS Project for Medical Science at Yonsei University. K.T.N. is supported by the Bio & Medical Technology Development Program of the National Research Foundation (NRF) funded by the Korean government (MSIT) (Nos. 2016M3A9D5A01952416 and 2021M3H9A1038083).

Publisher Copyright:
© 2022. Published by The Company of Biologists Ltd.

All Science Journal Classification (ASJC) codes

Neuroscience (miscellaneous)
Medicine (miscellaneous)
Immunology and Microbiology (miscellaneous)
Biochemistry, Genetics and Molecular Biology(all)

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10.1242/dmm.049632

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Jeong, H., Lee, Y. W., Park, I. H., Noh, H., Kim, S. H., Kim, J., Jeon, D., Jang, H. J., Oh, J., On, D., Uhm, C., Cho, K., Oh, H., Yoon, S., Seo, J. S., Kim, J. J., Seok, S. H., Lee, Y. J., Hong, S. M., ... Seong, J. K. (2022). Comparisonof the pathogenesis of SARS-CoV-2 infection inK18-hACE2 miceand Syrian golden hamstermodels. DMM Disease Models and Mechanisms, 15(11). https://doi.org/10.1242/dmm.049632

@article{8d71f1bb92544b6cba3b156c4ceb509c,

title = "Comparisonof the pathogenesis of SARS-CoV-2 infection inK18-hACE2 miceand Syrian golden hamstermodels",

abstract = "SARS-CoV-2, the etiological agentofCOVID-19, causeslife-threatening disease. This novel coronavirusenters host cellsvia the respiratory tract,promoting the formation ofsevere pulmonary lesions andsystemic disease. Few animal models can simulate the clinical signs and pathology ofCOVID-19patients.Diverse preclinical studies using K18-hACE2 mice and Syrian golden hamsters, which are highly permissive toSARS-CoV-2 in therespiratory tract, are emerging; however, the systemic pathogenesis and cellular tropism of these models remain obscure. We intranasally infected K18-hACE2 mice and Syrian golden hamsterswith SARS-CoV-2, and compared the clinical features, pathogenesis, cellular tropism,and infiltrated immune-cellsubsets. In K18-hACE2 mice, SARS-CoV-2 persistently replicated inalveolar cells and causedpulmonary and extra-pulmonary disease, resulting in fataloutcomes. Conversely, in Syrian golden hamsters, transient SARS-CoV-2infectioninbronchial cells causedreversible pulmonary disease,without mortality. Our findings provide comprehensive insightsinto thepathogenic spectrum of COVID-19 using pre-clinical models.",

author = "Haengdueng Jeong and Lee, {Youn Woo} and Park, {In Ho} and Hyuna Noh and Kim, {Sung Hee} and Jiseon Kim and Donghun Jeon and Jang, {Hui Jeong} and Jooyeon Oh and Dain On and Chanyang Uhm and Kyungrae Cho and Heeju Oh and Suhyeon Yoon and Seo, {Jung Seon} and Kim, {Jeong Jin} and Seok, {Sang Hyuk} and Lee, {Yu Jin} and Hong, {Seung Min} and An, {Se Hee} and Kim, {Seo Yeon} and Kim, {Young Been} and Hwang, {Ji Yeon} and Lee, {Hyo Jung} and Kim, {Hong Bin} and Jeong, {Dae Gwin} and Daesub Song and Manki Song and Park, {Man Seong} and Choi, {Kang Seuk} and Park, {Jun Won} and Seo, {Jun Young} and Yun, {Jun Won} and Shin, {Jeon Soo} and Lee, {Ho Young} and Nam, {Ki Taek} and Seong, {Je Kyung}",

note = "Funding Information: Funding: This project was supported by the Korea Mouse Phenotyping Project (NRF-2016M3A9D5A01952416) and by the Brain Korea 21 PLUS Project for Medical Science at Yonsei University. K.T.N. is supported by the Bio & Medical Technology Development Program of the National Research Foundation (NRF) funded by the Korean government (MSIT) (Nos. 2016M3A9D5A01952416 and 2021M3H9A1038083). Publisher Copyright: {\textcopyright} 2022. Published by The Company of Biologists Ltd.",

year = "2022",

month = nov,

doi = "10.1242/dmm.049632",

language = "English",

volume = "15",

journal = "DMM Disease Models and Mechanisms",

issn = "1754-8403",

publisher = "Company of Biologists Ltd",

number = "11",

}

Jeong, H, Lee, YW, Park, IH, Noh, H, Kim, SH, Kim, J, Jeon, D, Jang, HJ, Oh, J, On, D, Uhm, C, Cho, K, Oh, H, Yoon, S, Seo, JS, Kim, JJ, Seok, SH, Lee, YJ, Hong, SM, An, SH, Kim, SY, Kim, YB, Hwang, JY, Lee, HJ, Kim, HB, Jeong, DG, Song, D, Song, M, Park, MS, Choi, KS, Park, JW, Seo, JY, Yun, JW, Shin, JS, Lee, HY, Nam, KT & Seong, JK 2022, 'Comparisonof the pathogenesis of SARS-CoV-2 infection inK18-hACE2 miceand Syrian golden hamstermodels', DMM Disease Models and Mechanisms, vol. 15, no. 11. https://doi.org/10.1242/dmm.049632

TY - JOUR

T1 - Comparisonof the pathogenesis of SARS-CoV-2 infection inK18-hACE2 miceand Syrian golden hamstermodels

AU - Jeong, Haengdueng

AU - Lee, Youn Woo

AU - Park, In Ho

AU - Noh, Hyuna

AU - Kim, Sung Hee

AU - Kim, Jiseon

AU - Jeon, Donghun

AU - Jang, Hui Jeong

AU - Oh, Jooyeon

AU - On, Dain

AU - Uhm, Chanyang

AU - Cho, Kyungrae

AU - Oh, Heeju

AU - Yoon, Suhyeon

AU - Seo, Jung Seon

AU - Kim, Jeong Jin

AU - Seok, Sang Hyuk

AU - Lee, Yu Jin

AU - Hong, Seung Min

AU - An, Se Hee

AU - Kim, Seo Yeon

AU - Kim, Young Been

AU - Hwang, Ji Yeon

AU - Lee, Hyo Jung

AU - Kim, Hong Bin

AU - Jeong, Dae Gwin

AU - Song, Daesub

AU - Song, Manki

AU - Park, Man Seong

AU - Choi, Kang Seuk

AU - Park, Jun Won

AU - Seo, Jun Young

AU - Yun, Jun Won

AU - Shin, Jeon Soo

AU - Lee, Ho Young

AU - Nam, Ki Taek

AU - Seong, Je Kyung

N1 - Funding Information: Funding: This project was supported by the Korea Mouse Phenotyping Project (NRF-2016M3A9D5A01952416) and by the Brain Korea 21 PLUS Project for Medical Science at Yonsei University. K.T.N. is supported by the Bio & Medical Technology Development Program of the National Research Foundation (NRF) funded by the Korean government (MSIT) (Nos. 2016M3A9D5A01952416 and 2021M3H9A1038083). Publisher Copyright: © 2022. Published by The Company of Biologists Ltd.

PY - 2022/11

Y1 - 2022/11

N2 - SARS-CoV-2, the etiological agentofCOVID-19, causeslife-threatening disease. This novel coronavirusenters host cellsvia the respiratory tract,promoting the formation ofsevere pulmonary lesions andsystemic disease. Few animal models can simulate the clinical signs and pathology ofCOVID-19patients.Diverse preclinical studies using K18-hACE2 mice and Syrian golden hamsters, which are highly permissive toSARS-CoV-2 in therespiratory tract, are emerging; however, the systemic pathogenesis and cellular tropism of these models remain obscure. We intranasally infected K18-hACE2 mice and Syrian golden hamsterswith SARS-CoV-2, and compared the clinical features, pathogenesis, cellular tropism,and infiltrated immune-cellsubsets. In K18-hACE2 mice, SARS-CoV-2 persistently replicated inalveolar cells and causedpulmonary and extra-pulmonary disease, resulting in fataloutcomes. Conversely, in Syrian golden hamsters, transient SARS-CoV-2infectioninbronchial cells causedreversible pulmonary disease,without mortality. Our findings provide comprehensive insightsinto thepathogenic spectrum of COVID-19 using pre-clinical models.

AB - SARS-CoV-2, the etiological agentofCOVID-19, causeslife-threatening disease. This novel coronavirusenters host cellsvia the respiratory tract,promoting the formation ofsevere pulmonary lesions andsystemic disease. Few animal models can simulate the clinical signs and pathology ofCOVID-19patients.Diverse preclinical studies using K18-hACE2 mice and Syrian golden hamsters, which are highly permissive toSARS-CoV-2 in therespiratory tract, are emerging; however, the systemic pathogenesis and cellular tropism of these models remain obscure. We intranasally infected K18-hACE2 mice and Syrian golden hamsterswith SARS-CoV-2, and compared the clinical features, pathogenesis, cellular tropism,and infiltrated immune-cellsubsets. In K18-hACE2 mice, SARS-CoV-2 persistently replicated inalveolar cells and causedpulmonary and extra-pulmonary disease, resulting in fataloutcomes. Conversely, in Syrian golden hamsters, transient SARS-CoV-2infectioninbronchial cells causedreversible pulmonary disease,without mortality. Our findings provide comprehensive insightsinto thepathogenic spectrum of COVID-19 using pre-clinical models.

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U2 - 10.1242/dmm.049632

DO - 10.1242/dmm.049632

M3 - Article

C2 - 36222118

AN - SCOPUS:85141934558

SN - 1754-8403

VL - 15

JO - DMM Disease Models and Mechanisms

JF - DMM Disease Models and Mechanisms

IS - 11

ER -

Comparisonof the pathogenesis of SARS-CoV-2 infection inK18-hACE2 miceand Syrian golden hamstermodels

Abstract

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