tetano
Editor, Senior Moderator
J Infect Dis
. 2021 Dec 16;jiab595.
doi: 10.1093/infdis/jiab595. Online ahead of print.
Human T cells express Angiotensin Converting Enzyme 2 at levels sufficient to interact with the SARS-CoV-2 Spike protein
Jennifer L Welch[SUP] 1 2 3 [/SUP], Jinhua Xiang[SUP] 1 2 [/SUP], Qing Chang[SUP] 1 2 [/SUP], Jon C D Houtman[SUP] 2 3 [/SUP], Jack T Stapleton[SUP] 1 2 3 [/SUP]
Affiliations
Abstract
The pathogenesis of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is not completely understood. SARS-CoV-2 infection frequently causes significant immune function consequences including reduced T cell numbers and enhanced T cell exhaustion that contribute to disease severity. The extent to which T cell effects are directly mediated through infection or indirectly result from infection of respiratory-associated cells is unclear. We show that primary human T cells express sufficient levels of angiotensin converting enzyme 2 (ACE-2), the SARS-CoV-2 receptor, to mediate viral binding and entry into T cells. We further show that T cells exposed to SARS-CoV-2 particles demonstrate reduced proliferation and apoptosis compared to uninfected controls, indicating that direct interaction of SARS-CoV-2 with T cells may alter T cell growth, activation, and survival. Regulation of T cell activation and/or turnover by SARS-CoV-2 may contribute to impaired T cell function observed in patients with severe disease.
Keywords: ACE-2; SARS-CoV-2; T lymphocytes.
. 2021 Dec 16;jiab595.
doi: 10.1093/infdis/jiab595. Online ahead of print.
Human T cells express Angiotensin Converting Enzyme 2 at levels sufficient to interact with the SARS-CoV-2 Spike protein
Jennifer L Welch[SUP] 1 2 3 [/SUP], Jinhua Xiang[SUP] 1 2 [/SUP], Qing Chang[SUP] 1 2 [/SUP], Jon C D Houtman[SUP] 2 3 [/SUP], Jack T Stapleton[SUP] 1 2 3 [/SUP]
Affiliations
- PMID: 34918095
- DOI: 10.1093/infdis/jiab595
Abstract
The pathogenesis of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is not completely understood. SARS-CoV-2 infection frequently causes significant immune function consequences including reduced T cell numbers and enhanced T cell exhaustion that contribute to disease severity. The extent to which T cell effects are directly mediated through infection or indirectly result from infection of respiratory-associated cells is unclear. We show that primary human T cells express sufficient levels of angiotensin converting enzyme 2 (ACE-2), the SARS-CoV-2 receptor, to mediate viral binding and entry into T cells. We further show that T cells exposed to SARS-CoV-2 particles demonstrate reduced proliferation and apoptosis compared to uninfected controls, indicating that direct interaction of SARS-CoV-2 with T cells may alter T cell growth, activation, and survival. Regulation of T cell activation and/or turnover by SARS-CoV-2 may contribute to impaired T cell function observed in patients with severe disease.
Keywords: ACE-2; SARS-CoV-2; T lymphocytes.