TY - JOUR
T1 - Long COVID
T2 - pathophysiological factors and abnormalities of coagulation
AU - Turner, Simone
AU - Khan, M. Asad
AU - Putrino, David
AU - Woodcock, Ashley
AU - Kell, Douglas B.
AU - Pretorius, Etheresia
N1 - Funding Information:
D.B.K. thanks the Novo Nordisk Foundation for funding (grant NNF20CC0035580 ). The funders had no role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript. E.P. thanks the National Research Foundation of South Africa (grant number 142142 ) and South African Medical Research Council [self-initiated research (SIR) grant]. The content and findings reported and illustrated are the sole deduction, view and responsibility of the researchers and do not reflect the official position and sentiments of the funders.
Publisher Copyright:
© 2023 The Author(s)
PY - 2023/6
Y1 - 2023/6
N2 - Acute COVID-19 infection is followed by prolonged symptoms in approximately one in ten cases: known as Long COVID. The disease affects ~65 million individuals worldwide. Many pathophysiological processes appear to underlie Long COVID, including viral factors (persistence, reactivation, and bacteriophagic action of SARS CoV-2); host factors (chronic inflammation, metabolic and endocrine dysregulation, immune dysregulation, and autoimmunity); and downstream impacts (tissue damage from the initial infection, tissue hypoxia, host dysbiosis, and autonomic nervous system dysfunction). These mechanisms culminate in the long-term persistence of the disorder characterized by a thrombotic endothelialitis, endothelial inflammation, hyperactivated platelets, and fibrinaloid microclots. These abnormalities of blood vessels and coagulation affect every organ system and represent a unifying pathway for the various symptoms of Long COVID.
AB - Acute COVID-19 infection is followed by prolonged symptoms in approximately one in ten cases: known as Long COVID. The disease affects ~65 million individuals worldwide. Many pathophysiological processes appear to underlie Long COVID, including viral factors (persistence, reactivation, and bacteriophagic action of SARS CoV-2); host factors (chronic inflammation, metabolic and endocrine dysregulation, immune dysregulation, and autoimmunity); and downstream impacts (tissue damage from the initial infection, tissue hypoxia, host dysbiosis, and autonomic nervous system dysfunction). These mechanisms culminate in the long-term persistence of the disorder characterized by a thrombotic endothelialitis, endothelial inflammation, hyperactivated platelets, and fibrinaloid microclots. These abnormalities of blood vessels and coagulation affect every organ system and represent a unifying pathway for the various symptoms of Long COVID.
KW - cardiovascular outcomes
KW - clotting pathology
KW - endothelialitis
KW - long COVID
UR - http://www.scopus.com/inward/record.url?scp=85152888325&partnerID=8YFLogxK
U2 - 10.1016/j.tem.2023.03.002
DO - 10.1016/j.tem.2023.03.002
M3 - Review article
AN - SCOPUS:85152888325
SN - 1043-2760
VL - 34
SP - 321
EP - 344
JO - Trends in Endocrinology and Metabolism
JF - Trends in Endocrinology and Metabolism
IS - 6
ER -