Wild-type and innate immune-deficient mice are not susceptible to the Middle East respiratory syndrome coronavirus.
Identifieur interne : 001B49 ( PubMed/Curation ); précédent : 001B48; suivant : 001B50Wild-type and innate immune-deficient mice are not susceptible to the Middle East respiratory syndrome coronavirus.
Auteurs : Christopher M. Coleman [États-Unis] ; Krystal L. Matthews [États-Unis] ; Lindsay Goicochea [États-Unis] ; Matthew B. Frieman [États-Unis]Source :
- The Journal of general virology [ 1465-2099 ] ; 2014.
Descripteurs français
- KwdFr :
- MESH :
English descriptors
- KwdEn :
- MESH :
- pathogenicity : Coronaviridae.
- Animals, Disease Models, Animal, Disease Resistance, Humans, Mice, Mice, Inbred BALB C, Mice, Knockout, Mice, SCID.
Abstract
The Middle East respiratory syndrome coronavirus (MERS-CoV) is a newly emerging highly pathogenic virus causing almost 50 % lethality in infected individuals. The development of a small-animal model is critical for the understanding of this virus and to aid in development of countermeasures against MERS-CoV. We found that BALB/c, 129/SvEv and 129/SvEv STAT1 knockout mice are not permissive to MERS-CoV infection. The lack of infection may be due to the low level of mRNA and protein for the MERS-CoV receptor, dipeptidyl peptidase 4 (DPP4), in the lungs of mice. The low level of DPP4 in the lungs likely contributes to the lack of viral replication in these mouse models and suggests that a transgenic mouse model expressing DPP4 to higher levels is necessary to create a mouse model for MERS-CoV.
DOI: 10.1099/vir.0.060640-0
PubMed: 24197535
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The development of a small-animal model is critical for the understanding of this virus and to aid in development of countermeasures against MERS-CoV. We found that BALB/c, 129/SvEv and 129/SvEv STAT1 knockout mice are not permissive to MERS-CoV infection. The lack of infection may be due to the low level of mRNA and protein for the MERS-CoV receptor, dipeptidyl peptidase 4 (DPP4), in the lungs of mice. The low level of DPP4 in the lungs likely contributes to the lack of viral replication in these mouse models and suggests that a transgenic mouse model expressing DPP4 to higher levels is necessary to create a mouse model for MERS-CoV.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24197535</PMID><DateCompleted><Year>2014</Year><Month>03</Month><Day>21</Day></DateCompleted><DateRevised><Year>2020</Year><Month>03</Month><Day>05</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1465-2099</ISSN><JournalIssue CitedMedium="Internet"><Volume>95</Volume><Issue>Pt 2</Issue><PubDate><Year>2014</Year><Month>Feb</Month></PubDate></JournalIssue><Title>The Journal of general virology</Title><ISOAbbreviation>J. Gen. Virol.</ISOAbbreviation></Journal><ArticleTitle>Wild-type and innate immune-deficient mice are not susceptible to the Middle East respiratory syndrome coronavirus.</ArticleTitle><Pagination><MedlinePgn>408-412</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1099/vir.0.060640-0</ELocationID><Abstract><AbstractText>The Middle East respiratory syndrome coronavirus (MERS-CoV) is a newly emerging highly pathogenic virus causing almost 50 % lethality in infected individuals. The development of a small-animal model is critical for the understanding of this virus and to aid in development of countermeasures against MERS-CoV. We found that BALB/c, 129/SvEv and 129/SvEv STAT1 knockout mice are not permissive to MERS-CoV infection. The lack of infection may be due to the low level of mRNA and protein for the MERS-CoV receptor, dipeptidyl peptidase 4 (DPP4), in the lungs of mice. The low level of DPP4 in the lungs likely contributes to the lack of viral replication in these mouse models and suggests that a transgenic mouse model expressing DPP4 to higher levels is necessary to create a mouse model for MERS-CoV.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Coleman</LastName><ForeName>Christopher M</ForeName><Initials>CM</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, University of Maryland at Baltimore, Baltimore, MD, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Matthews</LastName><ForeName>Krystal L</ForeName><Initials>KL</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, University of Maryland at Baltimore, Baltimore, MD, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Goicochea</LastName><ForeName>Lindsay</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Pathology, Johns 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