Citation
Hoffmann, Markus, et al. "SARS-CoV-2 Cell Entry Depends On ACE2 and TMPRSS2 and Is Blocked By a Clinically Proven Protease Inhibitor." Cell, vol. 181, no. 2, 2020, pp. 271-280.e8.
Hoffmann M, Kleine-Weber H, Schroeder S, et al. SARS-CoV-2 Cell Entry Depends on ACE2 and TMPRSS2 and Is Blocked by a Clinically Proven Protease Inhibitor. Cell. 2020;181(2):271-280.e8.
Hoffmann, M., Kleine-Weber, H., Schroeder, S., Krüger, N., Herrler, T., Erichsen, S., Schiergens, T. S., Herrler, G., Wu, N. H., Nitsche, A., Müller, M. A., Drosten, C., & Pöhlmann, S. (2020). SARS-CoV-2 Cell Entry Depends on ACE2 and TMPRSS2 and Is Blocked by a Clinically Proven Protease Inhibitor. Cell, 181(2), 271-e8. https://doi.org/10.1016/j.cell.2020.02.052
Hoffmann M, et al. SARS-CoV-2 Cell Entry Depends On ACE2 and TMPRSS2 and Is Blocked By a Clinically Proven Protease Inhibitor. Cell. 2020 04 16;181(2):271-280.e8. PubMed PMID: 32142651.
TY - JOUR
T1 - SARS-CoV-2 Cell Entry Depends on ACE2 and TMPRSS2 and Is Blocked by a Clinically Proven Protease Inhibitor.
AU - Hoffmann,Markus,
AU - Kleine-Weber,Hannah,
AU - Schroeder,Simon,
AU - Krüger,Nadine,
AU - Herrler,Tanja,
AU - Erichsen,Sandra,
AU - Schiergens,Tobias S,
AU - Herrler,Georg,
AU - Wu,Nai-Huei,
AU - Nitsche,Andreas,
AU - Müller,Marcel A,
AU - Drosten,Christian,
AU - Pöhlmann,Stefan,
Y1 - 2020/03/05/
PY - 2020/02/06/received
PY - 2020/02/13/revised
PY - 2020/02/25/accepted
PY - 2020/3/7/pubmed
PY - 2020/4/24/medline
PY - 2020/3/7/entrez
KW - ACE2
KW - COVID-19
KW - SARS-CoV-2
KW - TMPRSS2
KW - coronavirus
KW - entry
KW - neutralization
KW - priming
KW - spike
SP - 271
EP - 280.e8
JF - Cell
JO - Cell
VL - 181
IS - 2
N2 - The recent emergence of the novel, pathogenic SARS-coronavirus 2 (SARS-CoV-2) in China and its rapid national and international spread pose a global health emergency. Cell entry of coronaviruses depends on binding of the viral spike (S) proteins to cellular receptors and on S protein priming by host cell proteases. Unravelling which cellular factors are used by SARS-CoV-2 for entry might provide insights into viral transmission and reveal therapeutic targets. Here, we demonstrate that SARS-CoV-2 uses the SARS-CoV receptor ACE2 for entry and the serine protease TMPRSS2 for S protein priming. A TMPRSS2 inhibitor approved for clinical use blocked entry and might constitute a treatment option. Finally, we show that the sera from convalescent SARS patients cross-neutralized SARS-2-S-driven entry. Our results reveal important commonalities between SARS-CoV-2 and SARS-CoV infection and identify a potential target for antiviral intervention.
SN - 1097-4172
UR - https://www.unboundmedicine.com/medline/citation/32142651/full_citation
L2 - https://linkinghub.elsevier.com/retrieve/pii/S0092-8674(20)30229-4
DB - PRIME
DP - Unbound Medicine
ER -