Convalescent COVID-19 patients are susceptible to endothelial dysfunction due to persistent immune activation
Florence WJ Chioh,
Siew-Wai Fong,
Barnaby E Young,
Kan-Xing Wu,
Anthony Siau,
Shuba Krishnan,
Yi-Hao Chan,
Guillaume Carissimo,
Louis LY Teo,
Fei Gao,
Ru San Tan,
Liang Zhong,
Angela S Koh,
Seow-Yen Tan,
Paul A Tambyah,
Laurent Renia,
Lisa FP Ng,
David C Lye,
Christine Cheung
Affiliations
Florence WJ Chioh
Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore, Singapore
Siew-Wai Fong
A*STAR ID Labs, Agency for Science, Technology and Research, Singapore, Singapore; Singapore Immunology Network, Agency for Science, Technology and Research, Singapore, Singapore; Department of Biological Sciences, National University of Singapore, Singapore, Singapore
Barnaby E Young
Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore, Singapore; National Centre for Infectious Diseases, Singapore, Singapore; Department of Infectious Diseases, Tan Tock Seng Hospital, Singapore, Singapore
Kan-Xing Wu
Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore, Singapore
Anthony Siau
Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore, Singapore
Shuba Krishnan
Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore, Singapore; Division of Clinical Microbiology, Department of Laboratory Medicine, Karolinska Institute, ANA Futura, Campus Flemingsberg, Stockholm, Sweden
A*STAR ID Labs, Agency for Science, Technology and Research, Singapore, Singapore; Singapore Immunology Network, Agency for Science, Technology and Research, Singapore, Singapore
Guillaume Carissimo
A*STAR ID Labs, Agency for Science, Technology and Research, Singapore, Singapore; Singapore Immunology Network, Agency for Science, Technology and Research, Singapore, Singapore
Louis LY Teo
National Heart Centre Singapore, Singapore, Singapore; Duke-NUS Medical School, Singapore, Singapore
Fei Gao
National Heart Centre Singapore, Singapore, Singapore; Duke-NUS Medical School, Singapore, Singapore
Ru San Tan
National Heart Centre Singapore, Singapore, Singapore; Duke-NUS Medical School, Singapore, Singapore
Liang Zhong
National Heart Centre Singapore, Singapore, Singapore; Duke-NUS Medical School, Singapore, Singapore
Angela S Koh
National Heart Centre Singapore, Singapore, Singapore; Duke-NUS Medical School, Singapore, Singapore
Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore, Singapore; A*STAR ID Labs, Agency for Science, Technology and Research, Singapore, Singapore; Singapore Immunology Network, Agency for Science, Technology and Research, Singapore, Singapore
Lisa FP Ng
A*STAR ID Labs, Agency for Science, Technology and Research, Singapore, Singapore; Singapore Immunology Network, Agency for Science, Technology and Research, Singapore, Singapore
David C Lye
Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore, Singapore; National Centre for Infectious Diseases, Singapore, Singapore; Department of Infectious Diseases, Tan Tock Seng Hospital, Singapore, Singapore; Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore
Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore, Singapore; Institute of Molecular and Cell Biology, Agency for Science, Technology and Research, Singapore, Singapore
Numerous reports of vascular events after an initial recovery from COVID-19 form our impetus to investigate the impact of COVID-19 on vascular health of recovered patients. We found elevated levels of circulating endothelial cells (CECs), a biomarker of vascular injury, in COVID-19 convalescents compared to healthy controls. In particular, those with pre-existing conditions (e.g., hypertension, diabetes) had more pronounced endothelial activation hallmarks than non-COVID-19 patients with matched cardiovascular risk. Several proinflammatory and activated T lymphocyte-associated cytokines sustained from acute infection to recovery phase, which correlated positively with CEC measures, implicating cytokine-driven endothelial dysfunction. Notably, we found higher frequency of effector T cells in our COVID-19 convalescents compared to healthy controls. The activation markers detected on CECs mapped to counter receptors found primarily on cytotoxic CD8+ T cells, raising the possibility of cytotoxic effector cells targeting activated endothelial cells. Clinical trials in preventive therapy for post-COVID-19 vascular complications may be needed.