Wild-type and innate immune-deficient mice are not susceptible to the Middle East respiratory syndrome coronavirus.
Identifieur interne : 001A22 ( Main/Exploration ); précédent : 001A21; suivant : 001A23Wild-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
Affiliations:
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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><affiliations><list><country><li>États-Unis</li></country><region><li>Maryland</li></region></list><tree><country name="États-Unis"><region name="Maryland"><name sortKey="Coleman, Christopher M" sort="Coleman, Christopher M" uniqKey="Coleman C" first="Christopher M" last="Coleman">Christopher M. 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