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Professor Roland Eils, head of the Digital Health Center at the Berlin Institute of Health at Charité (BIH), believes a possible explanation for this may lie in the way the virus attacks respiratory tract cells: “The virus requires several factors to gain entry into the cells. It attaches itself to the ACE2 receptor, which is found especially on cells in the upper respiratory tract (i.e., the throat and nasal mucosa). The ACE2 receptor is much rarer in lung cells. However, infection of the cells also depends on cofactors like the protease TMPRSS2. In contrast to the ACE2 receptor, TMPRSS2 is more abundant in lung cells than in upper airway cells.”

Eils continues: “It is now possible to imagine that the Omicron variant of the virus has optimized itself, through mutations in the spike protein, to be able to bind strongly to the ACE2 receptor. It consequently spreads much better in the upper respiratory tract, thus making it far more infectious than earlier variants. At the same time, it could be that the virus has as a result lost its ability to use the TMPRSS2 cofactor. That would make it difficult for the Omicron variant to infect lung cells, which have few ACE2 receptors and which are therefore critically dependent on the TMPRSS2 cofactor.”

This hypothesis is supported by six independent studies carried out in different model systems that consistently show that the Omicron variant efficiently infects cells in the upper respiratory tract but not cells in the lungs. This in turn would explain why only a few of those infected with Omicron go on to develop severe lung disease.

Eils emphasizes: “While this may be positive news, we unfortunately cannot give the all-clear. Due to the high number of cases in the current ‘Omicron wave,’ even a much smaller proportion of severely ill patients will still put a heavy burden on many people and on the healthcare system as a whole.”

Further information:

Current article in The New York Times about the Omicron variant:


Study from the research group of Roland Eils on the question of which cell types the SARS-CoV-2 virus infects:

Soeren Lukassen, Robert Lorenz Chua, Timo Trefzer, Nicolas C. Kahn, Marc A. Schneider, Thomas Muley, Hauke Winter, Michael Meister, Carmen Veith, Agnes W. Boots, Bianca P. Hennig, Michael Kreuter, Christian Conrad & Roland Eils: SARS‐CoV‐2 receptor ACE2 and TMPRSS2 are primarily expressed in bronchial transient secretory cells; EMBO Journal doi:10.15252/embj.20105114

Press release about the study: https://www.bihealth.org/en/notices/what-cells-does-the-novel-coronavirus-attack-1

Study on the susceptibility of various cell types in the respiratory tract to SARS-CoV-2 infection and the role of the immune system in COVID-19

Robert Lorenz Chua, Soeren Lukassen, Saskia Trump, Bianca P. Hennig, Daniel Wendisch, Fabian Pott, Olivia Debnath, Loreen Thürmann , Florian Kurth , Maria Theresa Völker, Julia Kazmierski, Bernd Timmermann, Sven Twardziok, Stefan Schneider, Felix Machleidt, Holger Müller-Redetzky, Melanie Maier, Alexander Krannich, Sein Schmidt, Felix Balzer, Johannes Liebig, Jennifer Loske, Norbert Suttorp, Jürgen Eils, Naveed Ishaque, Uwe Gerd Liebert, Christof von Kalle, Andreas Hocke, Martin Witzenrath, Christine Goffinet, Christian Drosten, Sven Laudi, Irina Lehmann, Christian Conrad, Leif-Erik Sander, & Roland Eils: COVID-19 severity correlates with airway epithelium–immune cell interactions identified by single-cell analysis; Nature Biotechnology https://doi.org/ 10.1038/s41587-020-0602-4

Press release about the study: https://www.bihealth.org/en/notices/the-dangerous-dual-role-of-the-immune-system-in-covid-19