2023/04/19 by Simone Turner, Asad Khan, M. Asad Khan +4 · 1 voice · 13 citations
Medicine · Neuroscience · #COVID-19 Clinical Research Studies #Long-Term Effects of COVID-19 #Neuroinflammation and Neurodegeneration Mechanisms
paper · pdf · doi:10.1016/j.tem.2023.03.002
openalex publication_date 2023/04/19 · openalex created_date 2025/10/10 · openalex updated_date 2026/07/29
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.