isolation-alveolar-type-ii-epithelial-cells-from-neonatal-juvenile

Isolation of Alveolar Type II Epithelial Cells from Neonatal, Juvenile, and Adult Murine Lungs Adaptable to Infectious Experimental Settings

Alveolar type II epithelial cells (AECII) critically contribute to immune regulation in the lung and thus are key elements orchestrating pulmonary ...

Otto-von-Guericke University Magdeburg

Helmholtz Centre for Infection Research

Route, origin & valence matter: towards sophisticated next-generation vaccines to cope with the COVID-19 pandemic.

The COVID-19 pandemic remains a global health threat and novel antiviral strategies are urgently needed. SARS-CoV-2 employs the cellular serine protease TMPRSS2 for entry into lung cells, and TMPRSS2 inhibitors are being developed for COVID-19 therapy. However, the SARS-CoV-2 Omicron variant, which currently dominates the pandemic, prefers the endo/lysosomal cysteine protease cathepsin L over TMPRSS2 for cell entry, raising doubts as to whether TMPRSS2 inhibitors would be suitable for the treatment of patients infected with the Omicron variant. Nevertheless, the contribution of TMPRSS2 to the spread of SARS-CoV-2 in the infected host is largely unclear. In this study, we show that the loss of TMPRSS2 strongly reduced the replication of the Beta variant in the nose, trachea and lung of C57BL/6 mice, and protected the animals from weight loss and disease. The infection of mice with the Omicron variant did not cause disease, as expected, but again, TMPRSS2 was essential for efficient viral spread in the upper and lower respiratory tract. These results identify the key role of TMPRSS2 in SARS-CoV-2 Beta and Omicron infection, and highlight TMPRSS2 as an attractive target for antiviral intervention.

Article	Year
Route, origin & valence matter: towards sophisticated next-generation vaccines to cope with the COVID-19 pandemic. Signal transduction and targeted therapy\| PubMed ID: 35705533	2022
TMPRSS2 Is Essential for SARS-CoV-2 Beta and Omicron Infection. Viruses\| PubMed ID: 36851486	2023

Lars Melcher

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