Infection with MERS-CoV causes lethal pneumonia in the common marmoset.
The availability of a robust disease model is essential for the development of countermeasures for Middle East respiratory syndrome coronavirus (MERS-CoV). While a rhesus macaque model of MERS-CoV has been established, the lack of uniform, severe disease in this model complicates the analysis of cou...
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Public Library of Science (PLoS)
2014
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oai:doaj.org-article:c18041d627c743fdbbfb5f3d8e37aa6c2021-11-25T05:46:09ZInfection with MERS-CoV causes lethal pneumonia in the common marmoset.1553-73661553-737410.1371/journal.ppat.1004250https://doaj.org/article/c18041d627c743fdbbfb5f3d8e37aa6c2014-08-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/25144235/?tool=EBIhttps://doaj.org/toc/1553-7366https://doaj.org/toc/1553-7374The availability of a robust disease model is essential for the development of countermeasures for Middle East respiratory syndrome coronavirus (MERS-CoV). While a rhesus macaque model of MERS-CoV has been established, the lack of uniform, severe disease in this model complicates the analysis of countermeasure studies. Modeling of the interaction between the MERS-CoV spike glycoprotein and its receptor dipeptidyl peptidase 4 predicted comparable interaction energies in common marmosets and humans. The suitability of the marmoset as a MERS-CoV model was tested by inoculation via combined intratracheal, intranasal, oral and ocular routes. Most of the marmosets developed a progressive severe pneumonia leading to euthanasia of some animals. Extensive lesions were evident in the lungs of all animals necropsied at different time points post inoculation. Some animals were also viremic; high viral loads were detected in the lungs of all infected animals, and total RNAseq demonstrated the induction of immune and inflammatory pathways. This is the first description of a severe, partially lethal, disease model of MERS-CoV, and as such will have a major impact on the ability to assess the efficacy of vaccines and treatment strategies as well as allowing more detailed pathogenesis studies.Darryl FalzaranoEmmie de WitFriederike FeldmannAngela L RasmussenAtsushi OkumuraXinxia PengMatthew J ThomasNeeltje van DoremalenElaine HaddockLee NagyRachel LaCasseTingting LiuJiang ZhuJason S McLellanDana P ScottMichael G KatzeHeinz FeldmannVincent J MunsterPublic Library of Science (PLoS)articleImmunologic diseases. AllergyRC581-607Biology (General)QH301-705.5ENPLoS Pathogens, Vol 10, Iss 8, p e1004250 (2014) |
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DOAJ |
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DOAJ |
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| topic |
Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5 |
| spellingShingle |
Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5 Darryl Falzarano Emmie de Wit Friederike Feldmann Angela L Rasmussen Atsushi Okumura Xinxia Peng Matthew J Thomas Neeltje van Doremalen Elaine Haddock Lee Nagy Rachel LaCasse Tingting Liu Jiang Zhu Jason S McLellan Dana P Scott Michael G Katze Heinz Feldmann Vincent J Munster Infection with MERS-CoV causes lethal pneumonia in the common marmoset. |
| description |
The availability of a robust disease model is essential for the development of countermeasures for Middle East respiratory syndrome coronavirus (MERS-CoV). While a rhesus macaque model of MERS-CoV has been established, the lack of uniform, severe disease in this model complicates the analysis of countermeasure studies. Modeling of the interaction between the MERS-CoV spike glycoprotein and its receptor dipeptidyl peptidase 4 predicted comparable interaction energies in common marmosets and humans. The suitability of the marmoset as a MERS-CoV model was tested by inoculation via combined intratracheal, intranasal, oral and ocular routes. Most of the marmosets developed a progressive severe pneumonia leading to euthanasia of some animals. Extensive lesions were evident in the lungs of all animals necropsied at different time points post inoculation. Some animals were also viremic; high viral loads were detected in the lungs of all infected animals, and total RNAseq demonstrated the induction of immune and inflammatory pathways. This is the first description of a severe, partially lethal, disease model of MERS-CoV, and as such will have a major impact on the ability to assess the efficacy of vaccines and treatment strategies as well as allowing more detailed pathogenesis studies. |
| format |
article |
| author |
Darryl Falzarano Emmie de Wit Friederike Feldmann Angela L Rasmussen Atsushi Okumura Xinxia Peng Matthew J Thomas Neeltje van Doremalen Elaine Haddock Lee Nagy Rachel LaCasse Tingting Liu Jiang Zhu Jason S McLellan Dana P Scott Michael G Katze Heinz Feldmann Vincent J Munster |
| author_facet |
Darryl Falzarano Emmie de Wit Friederike Feldmann Angela L Rasmussen Atsushi Okumura Xinxia Peng Matthew J Thomas Neeltje van Doremalen Elaine Haddock Lee Nagy Rachel LaCasse Tingting Liu Jiang Zhu Jason S McLellan Dana P Scott Michael G Katze Heinz Feldmann Vincent J Munster |
| author_sort |
Darryl Falzarano |
| title |
Infection with MERS-CoV causes lethal pneumonia in the common marmoset. |
| title_short |
Infection with MERS-CoV causes lethal pneumonia in the common marmoset. |
| title_full |
Infection with MERS-CoV causes lethal pneumonia in the common marmoset. |
| title_fullStr |
Infection with MERS-CoV causes lethal pneumonia in the common marmoset. |
| title_full_unstemmed |
Infection with MERS-CoV causes lethal pneumonia in the common marmoset. |
| title_sort |
infection with mers-cov causes lethal pneumonia in the common marmoset. |
| publisher |
Public Library of Science (PLoS) |
| publishDate |
2014 |
| url |
https://doaj.org/article/c18041d627c743fdbbfb5f3d8e37aa6c |
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