Yue Zhang, Vanthana Bharathi, Tatsuya Dokoshi, Jaime de Anda, Lauryn Tumey Ursery, Nikhil N Kulkarni, Yoshiyuki Nakamura, Jonathan Chen, Elizabeth W C Luo, Lamei Wang, Hua Xu, Alison Coady, Raymond Zurich, Michelle W Lee, Tsutomu Matsui, HongKyu Lee, Liana C Chan, Athena A Schepmoes, Mary S Lipton, Rui Zhao, Joshua N Adkins, Geremy C Clair, Lance R Thurlow, Jonathan C Schisler, Matthew C Wolfgang, Robert S Hagan, Michael R Yeaman, Thomas M Weiss, Xinhua Chen, Melody M H Li, Victor Nizet, Silvio Antoniak, Nigel Mackman, Richard L Gallo, Gerard C L Wong
It is unclear how severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection leads to the strong but ineffective inflammatory response that characterizes severe Coronavirus disease 2019 (COVID-19), with amplified immune activation in diverse cell types, including cells without angiotensin-converting enzyme 2 receptors necessary for infection. Proteolytic degradation of SARS-CoV-2 virions is a milestone in host viral clearance, but the impact of remnant viral peptide fragments from high viral loads is not known...
February 6, 2024: Proceedings of the National Academy of Sciences of the United States of America