Coronavirus MHV-A59 infects the lung and causes severe pneumonia in C57BL/6 mice.
Identifieur interne : 000E86 ( PubMed/Curation ); précédent : 000E85; suivant : 000E87Coronavirus MHV-A59 infects the lung and causes severe pneumonia in C57BL/6 mice.
Auteurs : Zhangsheng Yang [République populaire de Chine] ; Jun Du ; Gang Chen ; Jie Zhao ; Xuanming Yang ; Lishan Su ; Genhong Cheng ; Hong TangSource :
- Virologica Sinica [ 1995-820X ] ; 2014.
Descripteurs français
- KwdFr :
- Animaux, Cytokines (génétique), Cytokines (immunologie), Femelle, Humains, Infections à coronavirus (génétique), Infections à coronavirus (immunologie), Infections à coronavirus (virologie), Modèles animaux de maladie humaine, Mâle, Pneumopathie infectieuse (génétique), Pneumopathie infectieuse (immunologie), Pneumopathie infectieuse (virologie), Poumon (immunologie), Poumon (virologie), Souris, Souris de lignée C57BL, Virulence, Virus de l'hépatite murine (pathogénicité), Virus de l'hépatite murine (physiologie).
- MESH :
- génétique : Cytokines, Infections à coronavirus, Pneumopathie infectieuse.
- immunologie : Cytokines, Infections à coronavirus, Pneumopathie infectieuse, Poumon.
- pathogénicité : Virus de l'hépatite murine.
- physiologie : Virus de l'hépatite murine.
- virologie : Infections à coronavirus, Pneumopathie infectieuse, Poumon.
- Animaux, Femelle, Humains, Modèles animaux de maladie humaine, Mâle, Souris, Souris de lignée C57BL, Virulence.
English descriptors
- KwdEn :
- Animals, Coronavirus Infections (genetics), Coronavirus Infections (immunology), Coronavirus Infections (virology), Cytokines (genetics), Cytokines (immunology), Disease Models, Animal, Female, Humans, Lung (immunology), Lung (virology), Male, Mice, Mice, Inbred C57BL, Murine hepatitis virus (pathogenicity), Murine hepatitis virus (physiology), Pneumonia (genetics), Pneumonia (immunology), Pneumonia (virology), Virulence.
- MESH :
- chemical , genetics : Cytokines.
- genetics : Coronavirus Infections, Pneumonia.
- immunology : Coronavirus Infections, Cytokines, Lung, Pneumonia.
- pathogenicity : Murine hepatitis virus.
- physiology : Murine hepatitis virus.
- virology : Coronavirus Infections, Lung, Pneumonia.
- Animals, Disease Models, Animal, Female, Humans, Male, Mice, Mice, Inbred C57BL, Virulence.
Abstract
It remains challenging to develop animal models of lung infection and severe pneumonia by severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome cornavirus (MERS-CoV) without high level of containment. This inevitably hinders understanding of virushost interaction and development of appropriate countermeasures. Here we report that intranasal inoculation of sublethal doses of murine coronavirus mouse hepatitis virus A-59 (MHV-A59), a hepatic and neuronal tropic coronavirus, can induce acute pneumonia and severe lung injuries in C57BL/6 mice. Inflammatory leukocyte infiltrations, hemorrhages and fibrosis of alveolar walls can be observed 2-11 days after MHV-A59 infection. This pathological manifestation is associated with dramatical elevation of tissue IP-10 and IFN-γ and moderate increase of TNF-α and IL-1β, but inability of anti-viral type I interferon response. These results suggest that intranasal infection of MHV-A59 would serve as a surrogate mouse model of acute respiratory distress syndrome by SARS-CoV and MERS-CoV infections.
DOI: 10.1007/s12250-014-3530-y
PubMed: 25547683
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<front><div type="abstract" xml:lang="en">It remains challenging to develop animal models of lung infection and severe pneumonia by severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome cornavirus (MERS-CoV) without high level of containment. This inevitably hinders understanding of virushost interaction and development of appropriate countermeasures. Here we report that intranasal inoculation of sublethal doses of murine coronavirus mouse hepatitis virus A-59 (MHV-A59), a hepatic and neuronal tropic coronavirus, can induce acute pneumonia and severe lung injuries in C57BL/6 mice. Inflammatory leukocyte infiltrations, hemorrhages and fibrosis of alveolar walls can be observed 2-11 days after MHV-A59 infection. This pathological manifestation is associated with dramatical elevation of tissue IP-10 and IFN-γ and moderate increase of TNF-α and IL-1β, but inability of anti-viral type I interferon response. These results suggest that intranasal infection of MHV-A59 would serve as a surrogate mouse model of acute respiratory distress syndrome by SARS-CoV and MERS-CoV infections. </div>
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