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Immunological and transcriptional characterisation of SARS-CoV infected mouse lungs

Manuel Salzmann, Patrick Haider, Roberto Plasenzotti, Johann Wojta, Philipp Hohensinner
European Respiratory Journal 2021 58: PA3618; DOI: 10.1183/13993003.congress-2021.PA3618
Manuel Salzmann
1Division of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria
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  • For correspondence: manuel.salzmann@meduniwien.ac.at
Patrick Haider
1Division of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria
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Roberto Plasenzotti
2Division of Biomedical Research, Medical University of Vienna, Vienna, Austria
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Johann Wojta
1Division of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria
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Philipp Hohensinner
1Division of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria
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Abstract

Apart from clinical data, mouse models for SARS have helped advance our knowledge in fighting against COVID-19. We emphasised on a physiological model of infection and host-compatibility and used the murine coronavirus mCoV-A59, which belongs to the same subgroup as SARS-CoV-2. Thus, we could mimic asymptomatic infections with an immune response that results in major virus clearance at day 10 post infection. Using histology, multi-colour flow cytometry and RNAseq of mCoV infected lungs, we were able to detect an intriguing temporal interplay of innate and adaptive immunity in virus resolution.

Virus clearance was already evident after 4 days and RNAseq revealed the unexpectedly crucial role of innate immune cell regulation, being strongest regulated cellular pathway. Moreover, interferon type I signalling was also remarkably upregulated during this early phase; a hallmark of SARS-CoV infections and mainly produced by innate immune cells. Lung cell apoptosis was highest at day 10, at which we could also observe a distinct increase in cytotoxic CD8 T cells.

This indicates that successful, rapid SARS-CoV clearance depends mainly on innate immunity rather than on adaptive responses, while at a later phase recruited CD8 T cells contribute to lung tissue damage. This early innate immune response might explain the observed decline of SARS-CoV-2 antibodies in asymptomatic or mild infections. Thus, we highlight the importance to strengthen the innate immune system at the beginning of a SARS-CoV infection with the requirement to dampen CD8 T cell function. Lastly, our model allows screening of compounds modulating the innate and adaptive immunity during disease.

  • Immunology
  • Covid-19
  • Monocyte / Macrophage

Footnotes

Cite this article as: European Respiratory Journal 2021; 58: Suppl. 65, PA3618.

This abstract was presented at the 2021 ERS International Congress, in session “Prediction of exacerbations in patients with COPD”.

This is an ERS International Congress abstract. No full-text version is available. Further material to accompany this abstract may be available at www.ers-education.org (ERS member access only).

  • Copyright ©the authors 2021
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Immunological and transcriptional characterisation of SARS-CoV infected mouse lungs
Manuel Salzmann, Patrick Haider, Roberto Plasenzotti, Johann Wojta, Philipp Hohensinner
European Respiratory Journal Sep 2021, 58 (suppl 65) PA3618; DOI: 10.1183/13993003.congress-2021.PA3618

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Immunological and transcriptional characterisation of SARS-CoV infected mouse lungs
Manuel Salzmann, Patrick Haider, Roberto Plasenzotti, Johann Wojta, Philipp Hohensinner
European Respiratory Journal Sep 2021, 58 (suppl 65) PA3618; DOI: 10.1183/13993003.congress-2021.PA3618
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