- Roose, Jeroen;
- Hysenaj, Lisiena;
- Little, Samantha;
- Kulhanek, Kayla;
- Gbenedio, Oghenekevwe;
- Rodriguez, Lauren;
- Shen, Alan;
- Lone, Jean-Chrostophe;
- Lupin-Jimenez, Leonard;
- Bonser, Luke;
- Bahl, Kriti;
- Mick, Eran;
- Serwas, Nina;
- Vivianne, Dong;
- Li, Jack;
- Maishan, Mazharul;
- Matsumoto, Shotaro;
- Fragiadakis, Gabriela;
- Matthay, Michael;
- Jablons, David;
- Ott, Melanie;
- Langelier, Charles;
- Sil, Anita;
- Krummel, Matthew;
- Combes, Alexis;
- Erle, David;
- Kratz, Johannes;
- Roose, Jeroen
SARS coronavirus-2 (SARS-CoV-2) is causing a global pandemic with large variation in COVID-19 disease spectrum. SARS-CoV-2 infection requires host receptor ACE2 on lung epithelium, but epithelial underpinnings of variation are largely unknown. We capitalized on comprehensive organoid assays to report remarkable variation in SARS-CoV-2 infection rates of lung organoids from different subjects. Tropism is highest for TUBA- and MUC5AC-positive organoid cells, but levels of TUBA-, MUC5A-, or ACE2- positive cells do not predict infection rate. We identify surface molecule Tetraspanin 8 (TSPAN8) as novel mediator of SARS-CoV-2 infection, which is not downregulated by this specific virus. TSPAN8 levels, prior to infection, strongly correlate with infection rate and TSPAN8-blocking antibodies diminish SARS-CoV-2 infection. We propose TSPAN8 as novel functional biomarker and potential therapeutic target for COVID-19.