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SARS-CoV-2 infection of human ACE2-transgenic mice causes severe lung inflammation and impaired function
Open accessAbstract
Although animal models have been evaluated for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, none have fully recapitulated the lung disease phenotypes seen in humans who have been hospitalized. Here, we evaluate transgenic mice expressing the human angiotensin I-converting enzyme 2 (ACE2) receptor driven by the cytokeratin-18 (K18) gene promoter (K18-hACE2) as a model of SARS-CoV-2 infection. Intranasal inoculation of SARS-CoV-2 in K18-hACE2 mice results in high levels of viral infection in lungs, with spread to other organs. A decline in pulmonary function occurs 4 days after peak viral titer and correlates with infiltration of monocytes, neutrophils and activated T cells. SARS-CoV-2-infected lung tissues show a massively upregulated innate immune response with signatures of nuclear factor-κB-dependent, type I and II interferon signaling, and leukocyte activation pathways. Thus, the K18-hACE2 model of SARS-CoV-2 infection shares many features of severe COVID-19 infection and can be used to define the basis of lung disease and test immune and antiviral-based countermeasures.
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“In a humanized transgenic mouse model, ACE2 was expressed in the heart and virus replication detected, but they did not observe cardiac inflammation. 181”
From COVID-19, Myocarditis and Pericarditis (2023) · cites this paper as [181]
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“These transgenic mice have a human ACE2 receptor which is the major cell entry receptor for SARS-CoV-216,17.”
From Efficacy of an unmodified bivalent mRNA vaccine against SARS-CoV-2 variants in female small animal models (2023) · cites this paper as [17]
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“Consistent with prior reports of SARS- CoV-2 infection in the K18-hACE2 transgenic mouse model, 39,40,49 we observed significant morbidity (weight loss, clinical signs of infection, severe lung inflammation) and mortality in a large proportion of infected mice.”
MethodResultGlutamine metabolism is essential for coronavirus replication in host cells and in mice
Greene, K. S., Choi, A., Yang, N., Chen, M., Li, R., Qiu, Y., Ezzatpour, S., Rojas, K. S., Shen, J., Wilson, K. F., et al. (2024) · Journal of Biological Chemistry · doi:10.1016/j.jbc.2024.108063 · Cited by 6
Chakraborty, C., Lo, Y.-H., Bhattacharya, M., Das, A., & Wen, Z. (2025) · Molecular Therapy — Nucleic Acids · doi:10.1016/j.omtn.2025.102527 · Cited by 8
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COVID-19 and the Kidney: Recent Advances and Controversies
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Vaccination Provides Superior in vivo Recall Capacity of SARS-CoV-2 Specific Memory CD8 T Cells
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Exploring gut–lung axis crosstalk in SARS‐CoV‐2 infection: Insights from a hACE2 mouse model
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“34 – 38 Importantly, fecal viral activity is closely linked to gut microbiota composition.”
BackgroundImmune responses to SARS-CoV-2 infection in Humans and ACE2 humanized mice
Zhu, A., Chen, Z., Wang, Y., Zeng, Q., Sun, J., Zhuang, Z., Li, F., Zhao, J., Zhao, J., & Zhong, N. (2021) · Fundamental Research · doi:10.1016/j.fmre.2021.03.001 · Cited by 7
Immune responses to human respiratory coronaviruses infection in mouse models
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“We used K18-hACE2 transgenic (TG) mice as a model of SARS-CoV-2 infection (33).”
MethodSelf-citationMasters, E. A., Tang, W., Kang, I., Košíková, M., Hanks, J. H., Elkins, L., Kwon, H., Ortega‐Rodriguez, U., Gong, B., Mercer, K. E., et al. (2025) · Journal of Medical Virology · doi:10.1002/jmv.70506 · Cited by 5
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“This animal model has been previously characterized and shown to recapitulate key features of SARS- CoV-2 pathogenesis, including high viral replication in the lungs and, in some cases, neuroinvasion and CNS inflammation [12, 20, 21].”
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“We next assessed the immunogenicity and efficacy of RQ3013, RQ3019 and RQ3025 in the K18-hACE2 transgenic mouse strain which is susceptible to SARS-CoV-2 and suffers from lung injuries that mimic severe SARS-CoV-2 infection in humans [20–22].”
MethodNovel Pan-Coronavirus 3CL Protease Inhibitor MK-7845: Biological and Pharmacological Profiling
Álvarez, N., Adam, G. C., Howe, J. A., Sharma, V., Zimmerman, M. D., Dolgov, E., Rasheed, R., Nizar, F., Sahay, K., Nelson, A. M., et al. (2024) · Viruses · doi:10.3390/v16071158 · Cited by 5
“The K18-hACE2 transgenic mouse model is genetically engineered to express the human angiotensin-converting enzyme 2 (ACE2) receptor under the control of the cytokeratin-18 promoter, which enables susceptibility to SARS-CoV-2 infection [24].”
BackgroundResultThiede, J. M., Dick, J. K., Jarjour, N. N., Krishna, V. D., Qian, L. J., Sangala, J. A., Benzow, K. A., Karanjeet, K. B., Chin, S., Rainwater, O., et al. (2024) · ImmunoHorizons · doi:10.4049/immunohorizons.2400030 · Cited by 6
“These mice rapidly die following intranasal SARS-CoV-2 infection and show marked neurodissemination of the virus (16), which correlates with aberrant expression of the hACE2 transgene in the neuroepithelium and may contribute to the rapid death of infected K18-hACE2 mice (17).”
BackgroundDeMarco, J. K., Royal, J. M., Severson, W. E., Gabbard, J. D., Hume, S., Morton, J., Swope, K., Simpson, C. A., Shepherd, J. W., Bratcher, B., et al. (2021) · Vaccines · doi:10.3390/vaccines9111346 · Cited by 5
“Consistent with previous studies [24,27,28], we observed a significant increase in recruitment of these cells to the lungs in mice in the vehicle group (p = 0.”
ResultProspects of animal models and their application in studies on adaptive immunity to SARS-CoV-2
Wei, X., Rong, N., & Liu, J. (2022) · Frontiers in Immunology · doi:10.3389/fimmu.2022.993754 · Cited by 6
Efficacy of COVID-HIGIV in animal models of SARS-CoV-2 infection
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“[29] thoroughly analyzed lung inflammation and damage following SARSCoV-2 infection with the original virus at several time points, showing high levels of viral RNA and viral titers at several time points following infection, decline in pulmonary function, as well as extensive upregulation of the innate immune respons…”
BackgroundNeuromuscular defects after infection with a beta coronavirus in mice
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“Transgenic mice expressing human ACE2, regulated by the human cytokeratin 18 promoter in the epithelial cells, have been widely used to study SARS-CoV-2 pathogenesis [16,17].”
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Clever, S., Limpinsel, L., zu Natrup, C. M., Schünemann, L.-M., Beythien, G., Rosiak, M., Hülskötter, K., Gregor, K. M., Tuchel, T., Kalodimou, G., et al. (2024) · Viruses · doi:10.3390/v16030417 · Cited by 5
“…outcome of the K18-hACE2 mouse model and associated to the artificial expression of the human ACE2 receptor molecule in the brain [78], it might be interesting to test the emergency vaccination regimen in another animal model without the dominant brain manifestation and…”
Chong, Z., Karl, C. E., Halfmann, P., Kawaoka, Y., Winkler, E. S., Yu, J., & Diamond, M. (2022) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2022.01.21.477296 · Cited by 5
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“Although not naturally susceptible, genetically modified mice as well as mouse adapted SARS-CoV-2 viruses in wild type mice have also been used for SARS-CoV-2 preclinical modeling 39-41 .”
Sensing of cytoplasmic chromatin by cGAS activates innate immune response in SARS-CoV-2 infectionPreprint
Zhou, Z. L., Zhang, X., Lei, X., Xia, X., Jiao, T., Ma, R., Dong, X., Jiang, Q., Wang, W., Shi, Y., et al. (2021) · doi:10.21203/rs.3.rs-235742/v1 · Cited by 5
ACE2, From the Kidney to SARS-CoV-2: Donald Seldin Award Lecture 2023
BATLLE, D. C., Hassler, L., & Wysocki, J. A. (2024) · Hypertension · doi:10.1161/hypertensionaha.124.22064 · Cited by 4
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Novel Strategies for Developing Next-Generation Vaccines to Combat Infectious Viral Diseases
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“SARS-CoV-2 infection in hACE2 transgenic mice shows lung pathology similar to human pneumonia in severe infection cases [153,154].”
Lee, J., Case, J. B., Park, Y., Ravichandran, R., Asarnow, D. E., Tortorici, M. A., Brown, J. T., Sanapala, S., Carter, L. P., Baker, D. A., et al. (2026) · Communications Biology · doi:10.1038/s42003-025-09499-2 · Cited by 7
“To study the protective ef fi cacy of TRI2-2 in vivo against immune evasive SARS-CoV-2 Omicron variants, we intranasally inoculated highly susceptibleK18-hACE2mice 16 with10 4 FFUofBQ.1.1, XBB.1.5, orBA.2.86.”
InfluentialSelf-citationSARS-CoV-2 directly infects the inner ear and causes hearing dysfunction
Liu, X., Zong, Y., Liu, K., Shi, X., Zhao, Z., Shan, C., & Sun, Y. (2026) · Cell Reports · doi:10.1016/j.celrep.2026.117251 · Cited by 4
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“Such apparent reduction has also been previously reported in the context of influenza and SARS-Cov-2 infection (39, 40).”
Gunasekara, S., Selvan, M. T., Murphy, C. L., Shatnawi, S., Cowan, S. R., More, S., Ritchey, J. W., Miller, C., & Rudd, J. M. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms251810054 · Cited by 4
“in COVID-19 for and chemokines during SARS-CoV-2 infection orchestrates a robust immune response, pivotal in modulating and mitigating disease progression [32–35].”
BackgroundMODELING OF ENDOTHELIAL DYSFUNCTION AND SEARCH FOR ITS CIRCULATING BIOMARKERS
Shishkova, D. K., Frolov, A. V., Markova, V. E., Markova, Y. O., Kanonykina, A., Lazebnaya, A. A., Матвеева, В. Г., Torgunakova, E. A., & Кутихин, А. Г. (2024) · Complex Issues of Cardiovascular Diseases · doi:10.17802/2306-1278-2024-13-3s-173-190 · Cited by 4
Suppression of miR-155 Attenuates Lung Cytokine Storm Induced by SARS-CoV-2 Infection
Soni, D. K., Cabrera‐Luque, J., Kar, S., Ahmed, A., Sen, C., Devaney, J., & Biswas, R. (2025) · Journal of Interferon & Cytokine Research · doi:10.1089/jir.2024.0253 · Cited by 27
“Our fi ndings are consistence with previous studies which have reported low survival and signi fi cant weight loss in SARS-CoV-2-infected tg-mice (Jiang et al., 2020; Winkler et al., 2020).”
Saratale, G. D., Shin, H., Shinde, S. K., Kim, D.-Y., Saratale, R. G., Kadam, A. A., Kumar, M., Bahkali, A. H., Syed, A., & Ghodake, G. S. (2022) · Journal of Personalized Medicine · doi:10.3390/jpm12030349 · Cited by 5
“Besides this, it is interrelated with elevated levels of cytokines, mainly circulating ones [12], deep lymphopenia [13], and involved with extensive mononuclear cell infiltration in different organs, including lungs [14], spleen [15], heart [16], lymph nodes [17] and kidney [18], as observed in a post-mortem examinati…”
BackgroundTherapeutic Effect of C-Vx Substance in K18-hACE2 Transgenic Mice Infected with SARS-CoV-2
Polat, H. Ü., Abacı, İ., Tas, A. C., Aksoy, Ö., Öktelik, F. B., Yılmaz, V., Teki̇n, Ş., Okyar, A., Öncül, O., & Deniz, G. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms241511957 · Cited by 4
Improved survival of SARS COV-2-infected K18-hACE2 mice treated with adenosine A2AR agonist
Mann, B. J., Chhabra, P., Ma, M., Brovero, S. G., Hannan, R. T., Sturek, J. M., Jones, M., Linden, J. M., & Brayman, K. L. (2023) · Heliyon · doi:10.1016/j.heliyon.2023.e19226 · Cited by 4
“These cytokine and chemokine profiles in the vehicle treated infected mice are similar to other reports in K18-hACE2 mice [27,28].”
ResultBradshaw, C. M., Georgieva, T. G., Tankersley, T. N., Taylor-Doyle, T., Johnson, L., Uhrlaub, J. L., Besselsen, D. G., & Nikolich‐Žugich, J. (2024) · The Journal of Immunology · doi:10.4049/jimmunol.2300591 · Cited by 4
Jeong, G. U., Hwang, I., Lee, W., Choi, J. H., Yoon, G. Y., Kim, H. S., Yang, J., Kim, K.-C., Lee, J.-Y., Kim, S., et al. (2024) · Experimental & Molecular Medicine · doi:10.1038/s12276-024-01197-z · Cited by 4
Metzdorf, K., Jacobsen, H., 김연수, Alves, L. G. T., Kulkarni, U., Eschke, K., Chaudhry, M. Z., Hoffmann, M., Bertoglio, F., Ruschig, M., et al. (2024) · Frontiers in Immunology · doi:10.3389/fimmu.2024.1383086 · Cited by 4
Antiviral effect of cannabidiol on K18 ‐ hACE2 transgenic mice infected with SARS ‐ CoV ‐2
Polat, H. Ü., Yalcin, H. A., Köm, D., Aksoy, Ö., Abacı, İ., Tas, A. C., Serhatlı, M., & Onarıcı, S. (2024) · Journal of Cellular and Molecular Medicine · doi:10.1111/jcmm.70030 · Cited by 5
Muraoka, D., Meng, L.-M., Muto, O., Nakatsukasa, T., Deng, S.-T., Takashima, C., Yamaguchi, R., Sawada, S.-I., Hayakawa, H., Nguyen, T. T. N., et al. (2024) · npj Vaccines · doi:10.1038/s41541-024-00961-6 · Cited by 4
da Silva, K. N., Marim, F. M., Rocha, G. V., Costa‐Ferro, Z. S. M., França, L. S. D. A., Nonaka, C. K. V., Paredes, B. D., Rossi, E. A., Loiola, E. C., Adanho, C. S. A., et al. (2025) · Stem Cell Research & Therapy · doi:10.1186/s13287-024-04086-4 · Cited by 4
Singh, S. K., Kumar, A., & Sharma, H. (2022) · Recent Patents on Biotechnology · doi:10.2174/1872208316666220124101611 · Cited by 4
Long COVID: current status in Japan and knowledge about its molecular background
Matsunaga, A., Tsuzuki, S., Morioka, S., Ohmagari, N., & Ishizaka, Y. (2022) · Global Health & Medicine · doi:10.35772/ghm.2022.01013 · Cited by 6
Temporal Transcriptome Analysis of SARS-CoV-2-Infected Lung and Spleen in Human ACE2-Transgenic Mice
Kim, J. A., Kim, S.-H., Seo, J. S., Noh, H., Jeong, H., Kim, J., Jeon, D., Kim, J. J., Yoon, S., Yoon, S., et al. (2022) · Molecules and Cells · doi:10.14348/molcells.2022.0089 · Cited by 4
Brechbühl, J., Ferreira, F., Lopes, A. C., Corset, E., Gilliand, N., & Broillet, M.-C. (2023) · Viruses · doi:10.3390/v15020354 · Cited by 4
A suitable model to investigate acute neurological consequences of coronavirus infection
Pimenta, J. C., Oliveira, B. D. S., Lima, A. L. D., Machado, C. A., Lacerda, L. D. S. B., Rossi, L., Queiroz‐Junior, C. M., Souza‐Costa, L. P., Andrade, A. C. S. P., Gonçalves, M. R., et al. (2023) · Inflammation Research · doi:10.1007/s00011-023-01798-w · Cited by 4
Lee, K., Na, Y., Kim, M., Lee, D., Choi, J., Kim, G., & Kim, M.-S. (2024) · Pharmacology Research & Perspectives · doi:10.1002/prp2.1194 · Cited by 3
“The lung lesion of the K18-hACE2 transgenic mice model, for instance, exhibits a notable expression of ACE2, 36,38 which may clearly show how the Omicron infection altered the amount of ACE2.”
BackgroundLee, H., Lee, T. Y., Jeon, P., Kim, N., Kim, J., Yang, J., Kim, K.-C., & Lee, J.-Y. (2021) · Journal of Virological Methods · doi:10.1016/j.jviromet.2021.114306 · Cited by 4
A SARS CoV-2 nucleocapsid vaccine protects against distal viral disseminationPreprint
Class, J., Dangi, T., Richner, J. M., & Penaloza‐MacMaster, P. (2021) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2021.04.26.440920 · Cited by 4
Counoupas, C., Johansen, M. D., Stella, A. O., Nguyen, D. H., Ferguson, A. L., Aggarwal, A., Bhattacharyya, N. D., Grey, A., Patel, K., Siddiquee, R., et al. (2020) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2020.12.10.419044 · Cited by 4
Identification of ACE2 modifiers by CRISPR screeningPreprint
Sherman, E. J., Mirabelli, C., Tang, V. T., Khan, T. G., Kennedy, A. A., Graham, S. E., Willer, C. J., Tai, A. W., Sexton, J. Z., Wobus, C. E., et al. (2021) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2021.06.10.447768 · Cited by 4
“…abundance in HuH7 cells in our screen and as a proviral host factor for both SARS-CoV-2 and another ACE2-dependent coronavirus, HCoV-NL63, but not for other coronaviruses, HCoV-229E and HCoV-OC43, that use alternative cellular receptors (Figure 3C) (Hulswit et al., 2019; Yeager et al., 1992).”
BackgroundHilligan, K. L., Oyesola, O. O., Namasivayam, S., Howard, N., Clancy, C. S., Oland, S. D., Garza, N. L., Lafont, B. A. P., Johnson, R. F., Mayer-Barber, K. D., et al. (2022) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2022.11.09.515832 · Cited by 4
nanoCLAMP potently neutralizes SARS-CoV-2 and protects K18-hACE2 mice from infectionPreprint
Pagneux, Q., Garnier, N., Fabregue, M., Sharkaoui, S., Mazzoli, S., Engelmann, I., Boukherroub, R., Strecker, M., Cruz, E., Ducos, P. L., et al. (2023) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2023.04.03.535401 · Cited by 4
Abdallah, H. B., Marino, G., Idorn, M., Reinert, L. S., Bregnhøj, A., Paludan, S. R., & Johansen, C. (2024) · PLoS ONE · doi:10.1371/journal.pone.0310915 · Cited by 3
Culiat, C. T., Soni, D. K., Malkes, W., Wienhold, M. D., Zhang, L., Henry, E., Dragan, M., Kar, S., Angeles, D. M., Eaker, S. S., et al. (2024) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2024.151198 · Cited by 3
Rosiak, M., Schreiner, T., Beythien, G., Leitzen, E., Ulianytska, A., Allnoch, L., Becker, K., Michaely, L. M., Lockow, S., Clever, S., et al. (2025) · Viruses · doi:10.3390/v17070963 · Cited by 3
“…been shown to develop severe lung lesions following intranasal infection with SARS-CoV-2, including acute pneumonia, alveolar collapse, interstitial as well as perivascular and vascular immune cell infiltration, alveolar septal thickening, and proteinaceous debris in alveolar spaces [12,14,61–64].”
InfluentialMSC-Exosomes Carrying miRNA – Could they Enhance Tocilizumab Activity in Neuropathology of COVID-19?
Schultz, I. C., Bertoni, A. P. S., & Wink, M. R. (2022) · Stem Cell Reviews and Reports · doi:10.1007/s12015-022-10409-w · Cited by 3
Hansur, L., Louisa, M., & Wuyung, P. E. (2022) · AIP conference proceedings · doi:10.1063/5.0098285 · Cited by 3
Sangare, K., Liu, S., Selvaraj, P., Stauft, C. B., Starost, M. F., & Wang, T. T. (2024) · mSphere · doi:10.1128/msphere.00726-24 · Cited by 3
“SARS-CoV-2 infection of K18-hACE2 mice is usually lethal because of brain infection (12, 21, 34).”
A Primer on Proteomic Characterization of Intercellular Communication in a Virus Microenvironment
Kostas, J. C., Brainard, C. S., & Cristea, I. M. (2025) · Molecular & Cellular Proteomics · doi:10.1016/j.mcpro.2025.100913 · Cited by 4
“This excessive immune activation results in widespread in fl ammation and tissue damage, particularly in the lungs, and is associated with poor outcomes (96).”
Effector CD8 T cell differentiation in primary and breakthrough SARS-CoV-2 infection in mice
Kingstad-Bakke, B. A., Lee, W., Yount, B. L., Cleven, T., Park, H.-T., Sullivan, J. A., Baric, R. S., & Suresh, M. (2025) · Communications Biology · doi:10.1038/s42003-025-07820-7 · Cited by 5
“Studies using K18-hACE2 mice and wild-type strains of SARS-CoV-2 have shown greater severity in infection outcomes and complications compared to mouse-adapted strains, which provide a more controlled model for studying immune responses 43,68,69 .”
Rao, Y., Wang, T., Qin, C., Espinosa, B., Liu, Q., Ekanayake, A., Zhao, J., Savas, A. C., Zhang, C., Zarinfar, M., et al. (2025) · mBio · doi:10.1128/mbio.00649-25 · Cited by 18
Breathless Aftermath: Post-COVID-19 Pulmonary Fibrosis
Muthiah, D., Vaddadi, K., & Liu, L. (2025) · Viruses · doi:10.3390/v17081098 · Cited by 6
Ferreira, H. A. S., Guimarães, L. C., Costa, P. A. C., de Campos, C. L. V., Scalzo, S., Queiroz‐Junior, C. M., Figueiredo, M. M., Teixeira, M. M., Costa, V. V., & Guimarães, P. P. G. (2025) · International Journal of Pharmaceutics · doi:10.1016/j.ijpharm.2025.126073 · Cited by 5
Beyond TGFβ1 - novel treatment strategies targeting lung fibrosis
Sim, C., Lamanna, E., Cirnigliaro, F., & Lam, M. (2021) · The International Journal of Biochemistry & Cell Biology · doi:10.1016/j.biocel.2021.106090 · Cited by 3
Dysregulated Innate Immune and Inflammatory Responses in SARS-CoV-2 Infection and COVID-19 Severity
Ghosh, P., Nagaraja, S., Basavaraju, S., & Kesavardhana, S. (2021) · Critical Reviews in Immunology · doi:10.1615/critrevimmunol.2021039716 · Cited by 3
Dissecting Phenotype from Genotype with Clinical Isolates of SARS-CoV-2 First Wave Variants
Taylor, M. K., Williams, E. P., Xue, Y., Jenjaroenpun, P., Wongsurawat, T., Smith, A. P., Smith, A. M., Parvathareddy, J., Kong, Y., Vogel, P., et al. (2023) · Viruses · doi:10.3390/v15030611 · Cited by 3
“, IL-6) were present in the lung, which is similar to other reports for WA1/2020-infected K18-hACE2 mice [10,21].”
BackgroundResultde Souza, W. D. F., Zorzella-Pezavento, S. F. G., Ayupe, M. C., Salgado, C. L., Oliveira, B. D. C., Moreira, F., da Silva, G. W., Muraro, S. P., de Souza, G. F., Proença‐Módena, J. L., et al. (2023) · Cells · doi:10.3390/cells12071092 · Cited by 3
“Such inflammatory infiltrate displayed an impressive up-regulation of innate immunity markers, characterized by signatures of type I and II IFN and leukocyte activation pathways [11].”
BackgroundN-dihydrogalactochitosan reduces mortality in a lethal mouse model of SARS-CoV-2
Weiss, C. M., Liu, H., Ball, E. E., Hoover, A. R., Wong, T. S., Wong, C. F., Lam, S. S. K., Hode, T., Keel, M. K., Levenson, R. M., et al. (2023) · PLoS ONE · doi:10.1371/journal.pone.0289139 · Cited by 5
SARS‐CoV‐2 variants of concern elicit divergent early immune responses in hACE2 transgenic mice
Fricke, C., Pfaff, F., Ulrich, L., Halwe, N. J., Schön, J., Timm, L., Hoffmann, W., Rauch, S., Petsch, B., Hoffmann, D., et al. (2023) · European Journal of Immunology · doi:10.1002/eji.202250332 · Cited by 4
Kim, J., Youn, D., Choi, S.-H., Lee, Y. W., Sumberzul, D., Yoon, J., Lee, H., Bae, J. W., Noh, H., On, D., et al. (2023) · Experimental & Molecular Medicine · doi:10.1038/s12276-023-01110-0 · Cited by 3
“…enzyme 2 (hACE2) in epithelial lineages including airway epithelium under the control of the cytokeratin-18 promoter (K18), and the pathological signs of severe COVID-19, such as pneumonia and pulmonary dysfunction, has been reported to be recapitulated in these mice in several studies 5,31,32 .”
BackgroundSARS-CoV-2 decreases malaria severity in co-infected rodent models
Fraga, A., Mósca, A. F., Moita, D., Simas, J. P., Nunes‐Cabaço, H., & Prudêncio, M. (2023) · Frontiers in Cellular and Infection Microbiology · doi:10.3389/fcimb.2023.1307553 · Cited by 3
Metadata
- Authors
- Winkler, E. S., Bailey, A. L., Kafai, N. M., Nair, S., McCune, B. T., Yu, J., Fox, J. M., Chen, R. E., Earnest, J. T., Keeler, S. P., Ritter, J. H., Kang, L.-I., Dort, S., Robichaud, A., Head, R., Holtzman, M. J., & Diamond, M. S.
- Affiliations
- Washington University in St. Louis (US)
- Corresponding author
- Diamond, Michael S.
- ORCID
- Venue
- Nature Immunology
- Published
- 2020-08-24
- Volume
- 21
- Issue
- 11
- Pages
- 1327-1335
- ISSN
- 1529-2908 (ISSN-L)
- 1529-2916
- PMC
- PMC7578095
- OpenAlex
- W3080378920
- Cited by
- 901
- References
- 56
- Citations by year
- 2026: 55 · 2025: 72 · 2024: 124 · 2023: 131 · 2022: 234 · 2021: 252 · 2020: 32
- FWCI
- 21.20
- Type
- journal article
- Language
- en
- Update notices
- correction (2020-09-02)
- Open access
- bronze
- doi.org
- Locations
- Nature Immunology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases (75N93019C00062, R01 AI127828, R01 AI130591, R35 HL145242, F32 AI138392)
- United States Department of Defense | Defense Advanced Research Projects Agency (HR001117S0019)
- Topics
- Health Sciences › Medicine › Infectious Diseases › SARS-CoV-2 and COVID-19 Research
- Health Sciences › Medicine › Infectious Diseases › COVID-19 Clinical Research Studies
- Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
- Keywords
- SARS-CoV-2, COVID-19 pandemic, K18-hACE2 mice, animal model of COVID-19, lung inflammation, lung function decline, monocytes, neutrophils, T cell activation, innate immune response, interferon signaling, NF-κB signaling
- MeSH terms
- Betacoronavirus, Angiotensin-Converting Enzyme 2, COVID-19, SARS-CoV-2, Animals, Chlorocebus aethiops, Disease Models, Animal, Female, Humans, Immunity, Innate, Interferon Type I, Interferon-gamma, Peptidyl-Dipeptidase A, Leukocytes, Lymphocyte Activation, Male, Mice, Transgenic, Monocytes, Neutrophils, Pneumonia, Pneumonia, Viral, Promoter Regions, Genetic, T-Lymphocytes, Vero Cells, Virus Replication, NF-kappa B, Coronavirus Infections, Neutrophil Infiltration, Mice, Keratin-18, Pandemics
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