TMPRSS2 Contributes to Virus Spread and Immunopathology in the Airways of Murine Models after Coronavirus Infection.
Identifieur interne : 000A85 ( Main/Exploration ); précédent : 000A84; suivant : 000A86TMPRSS2 Contributes to Virus Spread and Immunopathology in the Airways of Murine Models after Coronavirus Infection.
Auteurs : Naoko Iwata-Yoshikawa [Japon] ; Tadashi Okamura [Japon] ; Yukiko Shimizu [Japon] ; Hideki Hasegawa [Japon] ; Makoto Takeda [Japon] ; Noriyo Nagata [Japon]Source :
- Journal of virology [ 1098-5514 ] ; 2019.
Descripteurs français
- KwdFr :
- Animaux, Cellules Vero, Coronavirus du syndrome respiratoire du Moyen-Orient (immunologie), Femelle, Glycoprotéine de spicule des coronavirus (métabolisme), Humains, Infections à coronavirus (immunologie), Infections à coronavirus (métabolisme), Infections à coronavirus (virologie), Lignée cellulaire, Modèles animaux de maladie humaine, Mâle, Poly I-C (métabolisme), Poumon (immunologie), Poumon (métabolisme), Poumon (virologie), Récepteur de type Toll-3 (métabolisme), Serine endopeptidases (métabolisme), Souris, Souris de lignée C57BL, Souris knockout, Souris transgéniques, Syndrome respiratoire aigu sévère (immunologie), Syndrome respiratoire aigu sévère (métabolisme), Syndrome respiratoire aigu sévère (virologie), Virus du SRAS.
- MESH :
- immunologie : Coronavirus du syndrome respiratoire du Moyen-Orient, Infections à coronavirus, Poumon, Syndrome respiratoire aigu sévère.
- métabolisme : Glycoprotéine de spicule des coronavirus, Infections à coronavirus, Poly I-C, Poumon, Récepteur de type Toll-3, Serine endopeptidases, Syndrome respiratoire aigu sévère.
- virologie : Infections à coronavirus, Poumon, Syndrome respiratoire aigu sévère.
- Animaux, Cellules Vero, Femelle, Humains, Lignée cellulaire, Modèles animaux de maladie humaine, Mâle, Souris, Souris de lignée C57BL, Souris knockout, Souris transgéniques, Virus du SRAS.
English descriptors
- KwdEn :
- Animals, Cell Line, Chlorocebus aethiops, Coronavirus Infections (immunology), Coronavirus Infections (metabolism), Coronavirus Infections (virology), Disease Models, Animal, Female, Humans, Lung (immunology), Lung (metabolism), Lung (virology), Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Mice, Transgenic, Middle East Respiratory Syndrome Coronavirus (immunology), Poly I-C (metabolism), SARS Virus, Serine Endopeptidases (metabolism), Severe Acute Respiratory Syndrome (immunology), Severe Acute Respiratory Syndrome (metabolism), Severe Acute Respiratory Syndrome (virology), Spike Glycoprotein, Coronavirus (metabolism), Toll-Like Receptor 3 (metabolism), Vero Cells.
- MESH :
- chemical , metabolism : Poly I-C, Serine Endopeptidases, Spike Glycoprotein, Coronavirus, Toll-Like Receptor 3.
- immunology : Coronavirus Infections, Lung, Middle East Respiratory Syndrome Coronavirus, Severe Acute Respiratory Syndrome.
- metabolism : Coronavirus Infections, Lung, Severe Acute Respiratory Syndrome.
- virology : Coronavirus Infections, Lung, Severe Acute Respiratory Syndrome.
- Animals, Cell Line, Chlorocebus aethiops, Disease Models, Animal, Female, Humans, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Mice, Transgenic, SARS Virus, Vero Cells.
Abstract
Transmembrane serine protease TMPRSS2 activates the spike protein of highly pathogenic human coronaviruses such as severe acute respiratory syndrome-related coronavirus (SARS-CoV) and Middle East respiratory syndrome-related coronavirus (MERS-CoV). In vitro, activation induces virus-cell membrane fusion at the cell surface. However, the roles of TMPRSS2 during coronavirus infection in vivo are unclear. Here, we used animal models of SARS-CoV and MERS-CoV infection to investigate the role of TMPRSS2. Th1-prone C57BL/6 mice and TMPRSS2-knockout (KO) mice were used for SARS-CoV infection, and transgenic mice expressing the human MERS-CoV receptor DPP4 (hDPP4-Tg mice) and TMPRSS2-KO hDPP4-Tg mice were used for MERS-CoV infection. After experimental infection, TMPRSS2-deficient mouse strains showed reduced body weight loss and viral kinetics in the lungs. Lack of TMPRSS2 affected the primary sites of infection and virus spread within the airway, accompanied by less severe immunopathology. However, TMPRSS2-KO mice showed weakened inflammatory chemokine and/or cytokine responses to intranasal stimulation with poly(I·C), a Toll-like receptor 3 agonist. In conclusion, TMPRSS2 plays a crucial role in viral spread within the airway of murine models infected by SARS-CoV and MERS-CoV and in the resulting immunopathology.IMPORTANCE Broad-spectrum antiviral drugs against highly pathogenic coronaviruses and other emerging viruses are desirable to enable a rapid response to pandemic threats. Transmembrane protease serine type 2 (TMPRSS2), a protease belonging to the type II transmembrane serine protease family, cleaves the coronavirus spike protein, making it a potential therapeutic target for coronavirus infections. Here, we examined the role of TMPRSS2 using animal models of SARS-CoV and MERS-CoV infection. The results suggest that lack of TMPRSS2 in the airways reduces the severity of lung pathology after infection by SARS-CoV and MERS-CoV. Taken together, the results will facilitate development of novel targets for coronavirus therapy.
DOI: 10.1128/JVI.01815-18
PubMed: 30626688
Affiliations:
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Le document en format XML
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<term>Coronavirus Infections (metabolism)</term>
<term>Coronavirus Infections (virology)</term>
<term>Disease Models, Animal</term>
<term>Female</term>
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<term>Syndrome respiratoire aigu sévère (virologie)</term>
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<term>Humains</term>
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<front><div type="abstract" xml:lang="en">Transmembrane serine protease TMPRSS2 activates the spike protein of highly pathogenic human coronaviruses such as severe acute respiratory syndrome-related coronavirus (SARS-CoV) and Middle East respiratory syndrome-related coronavirus (MERS-CoV). <i>In vitro</i>
, activation induces virus-cell membrane fusion at the cell surface. However, the roles of TMPRSS2 during coronavirus infection <i>in vivo</i>
are unclear. Here, we used animal models of SARS-CoV and MERS-CoV infection to investigate the role of TMPRSS2. Th1-prone C57BL/6 mice and TMPRSS2-knockout (KO) mice were used for SARS-CoV infection, and transgenic mice expressing the human MERS-CoV receptor DPP4 (hDPP4-Tg mice) and TMPRSS2-KO hDPP4-Tg mice were used for MERS-CoV infection. After experimental infection, TMPRSS2-deficient mouse strains showed reduced body weight loss and viral kinetics in the lungs. Lack of TMPRSS2 affected the primary sites of infection and virus spread within the airway, accompanied by less severe immunopathology. However, TMPRSS2-KO mice showed weakened inflammatory chemokine and/or cytokine responses to intranasal stimulation with poly(I·C), a Toll-like receptor 3 agonist. In conclusion, TMPRSS2 plays a crucial role in viral spread within the airway of murine models infected by SARS-CoV and MERS-CoV and in the resulting immunopathology.<b>IMPORTANCE</b>
Broad-spectrum antiviral drugs against highly pathogenic coronaviruses and other emerging viruses are desirable to enable a rapid response to pandemic threats. Transmembrane protease serine type 2 (TMPRSS2), a protease belonging to the type II transmembrane serine protease family, cleaves the coronavirus spike protein, making it a potential therapeutic target for coronavirus infections. Here, we examined the role of TMPRSS2 using animal models of SARS-CoV and MERS-CoV infection. The results suggest that lack of TMPRSS2 in the airways reduces the severity of lung pathology after infection by SARS-CoV and MERS-CoV. Taken together, the results will facilitate development of novel targets for coronavirus therapy.</div>
</front>
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