Seminars in Immunology, Journal Year: 2024, Volume and Issue: 72, P. 101873 - 101873
Published: March 1, 2024
Language: Английский
Seminars in Immunology, Journal Year: 2024, Volume and Issue: 72, P. 101873 - 101873
Published: March 1, 2024
Language: Английский
Neuron, Journal Year: 2022, Volume and Issue: 110(21), P. 3484 - 3496
Published: Oct. 7, 2022
Persistent neurological and neuropsychiatric symptoms affect a substantial fraction of people after COVID-19 represent major component the post-acute syndrome, also known as long COVID. Here, we review what is understood about pathobiology impact on CNS discuss possible neurobiological underpinnings cognitive affecting survivors. We propose chief mechanisms that may contribute to this emerging health crisis.
Language: Английский
Citations
297Nature reviews. Immunology, Journal Year: 2023, Volume and Issue: 23(10), P. 618 - 634
Published: July 11, 2023
Language: Английский
Citations
261Frontiers in Medicine, Journal Year: 2023, Volume and Issue: 10
Published: Jan. 20, 2023
Purpose Long COVID, also known as post-acute sequelae of COVID-19, refers to the constellation long-term symptoms experienced by people suffering persistent for one or more months after SARS-CoV-2 infection. Blood biomarkers can be altered in long COVID patients; however, associated with and their roles disease progression remain undetermined. This study aims systematically evaluate blood that may act indicators therapeutic targets COVID. Methods A systematic literature review PubMed, Embase, CINAHL was performed on 18 August 2022. The search keywords COVID-19 were used filter out eligible studies, which then carefully evaluated. Results Identified from 28 studies representing six biological classifications, 113 significantly COVID: (1) Cytokine/Chemokine (38, 33.6%); (2) Biochemical markers (24, 21.2%); (3) Vascular (20, 17.7%); (4) Neurological (6, 5.3%); (5) Acute phase protein (5, 4.4%); (6) Others 17.7%). Compared healthy control recovered patients without symptoms, 79 increased, 29 decreased, 5 required further determination patients. Of these, up-regulated Interleukin 6, C-reactive protein, tumor necrosis factor alpha might serve potential diagnostic Moreover, neurological exhibited higher levels neurofilament light chain glial fibrillary acidic whereas those pulmonary a level transforming growth beta. Conclusion present elevated inflammatory initial Our found significant associations between specific symptoms. Further investigations are warranted identify core set diagnose manage clinical practice.
Language: Английский
Citations
146The Lancet Respiratory Medicine, Journal Year: 2023, Volume and Issue: 11(8), P. 709 - 725
Published: May 19, 2023
Language: Английский
Citations
95Nature Medicine, Journal Year: 2023, Volume and Issue: 29(10), P. 2498 - 2508
Published: Aug. 31, 2023
Post-COVID cognitive deficits, including 'brain fog', are clinically complex, with both objective and subjective components. They common debilitating, can affect the ability to work, yet their biological underpinnings remain unknown. In this prospective cohort study of 1,837 adults hospitalized COVID-19, we identified two distinct biomarker profiles measured during acute admission, which predict outcomes 6 12 months after COVID-19. A first profile links elevated fibrinogen relative C-reactive protein deficits. second D-dimer deficits occupational impact. This was mediated by fatigue shortness breath. Neither significantly depression or anxiety. Results were robust across secondary analyses. replicated, specificity COVID-19 tested, in a large-scale electronic health records dataset. These findings provide insights into heterogeneous biology post-COVID
Language: Английский
Citations
65International Journal of Molecular Sciences, Journal Year: 2023, Volume and Issue: 24(19), P. 14876 - 14876
Published: Oct. 4, 2023
SARS-CoV-2 infection, discovered and isolated in Wuhan City, Hubei Province, China, causes acute atypical respiratory symptoms has led to profound changes our lives. COVID-19 is characterized by a wide range of complications, which include pulmonary embolism, thromboembolism arterial clot formation, arrhythmias, cardiomyopathy, multiorgan failure, more. The disease caused worldwide pandemic, despite various measures such as social distancing, preventive strategies, therapeutic approaches, the creation vaccines, novel coronavirus infection (COVID-19) still hides many mysteries for scientific community. Oxidative stress been suggested play an essential role pathogenesis COVID-19, determining free radical levels patients with may provide insight into severity. generation abnormal oxidants under COVID-19-induced cytokine storm irreversible oxidation macromolecules subsequent damage cells, tissues, organs. Clinical studies have shown that oxidative initiates endothelial damage, increases risk complications post-COVID-19 or long-COVID-19 cases. This review describes radicals mediation mitochondrial dysfunction.
Language: Английский
Citations
64Journal of Thrombosis and Haemostasis, Journal Year: 2023, Volume and Issue: 21(8), P. 2020 - 2031
Published: May 11, 2023
Language: Английский
Citations
51Journal of the American College of Cardiology, Journal Year: 2023, Volume and Issue: 81(18), P. 1747 - 1762
Published: March 6, 2023
Language: Английский
Citations
50Nature, Journal Year: 2024, Volume and Issue: 633(8031), P. 905 - 913
Published: Aug. 28, 2024
Abstract Life-threatening thrombotic events and neurological symptoms are prevalent in COVID-19 persistent patients with long COVID experiencing post-acute sequelae of SARS-CoV-2 infection 1–4 . Despite the clinical evidence 1,5–7 , underlying mechanisms coagulopathy its consequences inflammation neuropathology remain poorly understood treatment options insufficient. Fibrinogen, central structural component blood clots, is abundantly deposited lungs brains COVID-19, correlates disease severity a predictive biomarker for post-COVID-19 cognitive deficits 1,5,8–10 Here we show that fibrin binds to spike protein, forming proinflammatory clots drive systemic thromboinflammation COVID-19. Fibrin, acting through inflammatory domain, required oxidative stress macrophage activation lungs, whereas it suppresses natural killer cells, after infection. Fibrin promotes neuroinflammation neuronal loss infection, as well innate immune brain independently active A monoclonal antibody targeting domain provides protection from microglial injury, lung Thus, drives fibrin-targeting immunotherapy may represent therapeutic intervention acute COVID.
Language: Английский
Citations
26Frontiers in Immunology, Journal Year: 2024, Volume and Issue: 15
Published: March 4, 2024
The coronavirus disease 2019 (COVID-19) pandemic caused by SARS-CoV-2 has been defined as the greatest global health and socioeconomic crisis of modern times. While most people recover after being infected with virus, a significant proportion them continue to experience issues weeks, months even years acute infection SARS-CoV-2. This persistence clinical symptoms in individuals for at least three onset or emergence new lasting more than two months, without any other explanation alternative diagnosis have named long COVID, long-haul post-COVID-19 conditions, chronic post-acute sequelae (PASC). Long COVID characterized constellation disorders that vary widely their manifestations. Further, mechanisms underlying are not fully understood, which hamper efficient treatment options. review describes predictors common related COVID's effects on central peripheral nervous system organs tissues. Furthermore, transcriptional markers, molecular signaling pathways risk factors such sex, age, pre-existing condition, hospitalization during phase COVID-19, vaccination, lifestyle presented. Finally, recommendations patient rehabilitation management, well therapeutical approaches discussed. Understanding complexity this disease, its across multiple organ systems overlapping pathologies possible paramount developing diagnostic tools treatments.
Language: Английский
Citations
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