Long COVID: major findings, mechanisms and recommendations

Nature Reviews Microbiology, Journal Year: 2023, Volume and Issue: 21(3), P. 133 - 146

Published: Jan. 13, 2023

Language: Английский

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Insights from myalgic encephalomyelitis/chronic fatigue syndrome may help unravel the pathogenesis of postacute COVID-19 syndrome

Trends in Molecular Medicine, Journal Year: 2021, Volume and Issue: 27(9), P. 895 - 906

Published: June 7, 2021

Language: Английский

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TRP (transient receptor potential) ion channel family: structures, biological functions and therapeutic interventions for diseases

Signal Transduction and Targeted Therapy, Journal Year: 2023, Volume and Issue: 8(1)

Published: July 5, 2023

Abstract Transient receptor potential (TRP) channels are sensors for a variety of cellular and environmental signals. Mammals express total 28 different TRP channel proteins, which can be divided into seven subfamilies based on amino acid sequence homology: TRPA (Ankyrin), TRPC (Canonical), TRPM (Melastatin), TRPML (Mucolipin), TRPN (NO-mechano-potential, NOMP), TRPP (Polycystin), TRPV (Vanilloid). They class ion found in numerous tissues cell types permeable to wide range cations such as Ca 2+ , Mg Na + K others. responsible various sensory responses including heat, cold, pain, stress, vision taste activated by number stimuli. Their predominantly location the surface, their interaction with physiological signaling pathways, unique crystal structure make TRPs attractive drug targets implicate them treatment diseases. Here, we review history discovery, summarize structures functions family, highlight current understanding role pathogenesis human disease. Most importantly, describe channel-related therapeutic interventions diseases limitations targeting clinical applications.

Language: Английский

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ME/CFS and Long COVID share similar symptoms and biological abnormalities: road map to the literature

Frontiers in Medicine, Journal Year: 2023, Volume and Issue: 10

Published: June 2, 2023

Some patients remain unwell for months after "recovering" from acute COVID-19. They develop persistent fatigue, cognitive problems, headaches, disrupted sleep, myalgias and arthralgias, post-exertional malaise, orthostatic intolerance other symptoms that greatly interfere with their ability to function can leave some people housebound disabled. The illness (Long COVID) is similar myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) as well persisting illnesses follow a wide variety of infectious agents following major traumatic injury. Together, these are projected cost the U.S. trillions dollars. In this review, we first compare ME/CFS Long COVID, noting considerable similarities few differences. We then in extensive detail underlying pathophysiology two conditions, focusing on abnormalities central autonomic nervous system, lungs, heart, vasculature, immune gut microbiome, energy metabolism redox balance. This comparison highlights how strong evidence each abnormality, illness, helps set priorities future investigation. review provides current road map literature biology both illnesses.

Language: Английский

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Long COVID and the cardiovascular system—elucidating causes and cellular mechanisms in order to develop targeted diagnostic and therapeutic strategies: a joint Scientific Statement of the ESC Working Groups on Cellular Biology of the Heart and Myocardial and Pericardial Diseases

Cardiovascular Research, Journal Year: 2022, Volume and Issue: 119(2), P. 336 - 356

Published: July 25, 2022

Abstract Long COVID has become a world-wide, non-communicable epidemic, caused by long-lasting multiorgan symptoms that endure for weeks or months after SARS-CoV-2 infection already subsided. This scientific document aims to provide insight into the possible causes and therapeutic options available cardiovascular manifestations of long COVID. In addition chronic fatigue, which is common symptom COVID, patients may present with chest pain, ECG abnormalities, postural orthostatic tachycardia, newly developed supraventricular ventricular arrhythmias. Imaging heart vessels provided evidence chronic, post-infectious perimyocarditis consequent left right failure, arterial wall inflammation, microthrombosis in certain patient populations. Better understanding underlying cellular molecular mechanisms will aid development effective treatment strategies its manifestations. A number have been proposed, including those involving direct effects on myocardium, microthrombotic damage endothelium, persistent inflammation. Unfortunately, existing circulating biomarkers, coagulation, inflammatory markers, are not highly predictive either presence outcome when measured 3 infection. Further studies needed understand mechanisms, identify specific guide future preventive treatments address sequelae.

Language: Английский

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COVID-19 2022 update: transition of the pandemic to the endemic phase

Human Genomics, Journal Year: 2022, Volume and Issue: 16(1)

Published: June 1, 2022

Abstract COVID-19, which is caused by the SARS-CoV-2, has ravaged world for past 2 years. Here, we review current state of research into disease with focus on its history, human genetics and genomics transition from pandemic to endemic phase. We are particularly concerned lack solid information initial phases that highlighted necessity better preparation face similar future threats. On other hand, gratified progress genetic susceptibility investigations believe now time explore The latter will require worldwide vigilance cooperation, especially in emerging countries. In phase, vaccination rates have lagged developed countries should assist, as warranted, bolstering worldwide. also discuss status vaccines outlook COVID-19.

Language: Английский

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Long COVID science, research and policy

Nature Medicine, Journal Year: 2024, Volume and Issue: 30(8), P. 2148 - 2164

Published: Aug. 1, 2024

Long COVID represents the constellation of post-acute and long-term health effects caused by SARS-CoV-2 infection; it is a complex, multisystem disorder that can affect nearly every organ system be severely disabling. The cumulative global incidence long around 400 million individuals, which estimated to have an annual economic impact approximately $1 trillion-equivalent about 1% economy. Several mechanistic pathways are implicated in COVID, including viral persistence, immune dysregulation, mitochondrial dysfunction, complement endothelial inflammation microbiome dysbiosis. devastating impacts on individual lives and, due its complexity prevalence, also has major ramifications for systems economies, even threatening progress toward achieving Sustainable Development Goals. Addressing challenge requires ambitious coordinated-but so far absent-global research policy response strategy. In this interdisciplinary review, we provide synthesis state scientific evidence assess human health, systems, economy metrics, forward-looking roadmap.

Language: Английский

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“LONG COVID”—A hypothesis for understanding the biological basis and pharmacological treatment strategy

Pharmacology Research & Perspectives, Journal Year: 2022, Volume and Issue: 10(1)

Published: Jan. 13, 2022

Abstract Infection of humans with SARS‐CoV‐2 virus causes a disease known colloquially as “COVID‐19” symptoms ranging from asymptomatic to severe pneumonia. Initial pathology is due the binding ACE‐2 protein on endothelial cells lining blood vessels and entering these in order replicate. Viral replication oxidative stress elevated levels reactive oxygen species. Many (~60%) infected people appear have eliminated their body after 28 days resume normal activity. However, significant proportion (~40%) experience variety (loss smell and/or taste, fatigue, cough, aching pain, “brain fog,” insomnia, shortness breath, tachycardia) 12 weeks are diagnosed syndrome named “LONG COVID.” Longitudinal clinical studies group subjects who were been compared non‐infected matched subjects. A cohort can be identified by battery cytokine markers persistent, low level grade inflammation often self‐report two or more troubling symptoms. There no drug that will relieve effectively. It hypothesized drugs activate intracellular transcription factor, nuclear factor erythroid‐derived 2‐like 2 (NRF2) may increase expression enzymes synthesize antioxidant, glutathione quench free radicals causing stress. The hormone melatonin has an activator NRF2 relatively safe chemical for most ingest chronically. Thus, it option consideration re‐purposing COVID” experiencing depression, fog” but not tachycardia. Appropriately designed trials required evaluate melatonin.

Language: Английский

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Deficient butyrate-producing capacity in the gut microbiome is associated with bacterial network disturbances and fatigue symptoms in ME/CFS

Cell Host & Microbe, Journal Year: 2023, Volume and Issue: 31(2), P. 288 - 304.e8

Published: Feb. 1, 2023

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is characterized by unexplained debilitating fatigue, cognitive dysfunction, gastrointestinal disturbances, and orthostatic intolerance. Here, we report a multi-omic analysis of geographically diverse cohort 106 cases 91 healthy controls that revealed differences in gut microbiome diversity, abundances, functional pathways, interactions. Faecalibacterium prausnitzii Eubacterium rectale, which are both recognized as abundant, health-promoting butyrate producers the human gut, were reduced ME/CFS. Functional metagenomics, qPCR, metabolomics fecal short-chain fatty acids confirmed deficient microbial capacity for synthesis. Microbiome-based machine learning classifier models robust to geographic variation generalizable validation cohort. The abundance was inversely associated with severity. These findings demonstrate nature dysbiosis underlying network disturbance ME/CFS, providing possible targets disease classification therapeutic trials.

Language: Английский

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The role of oxidative stress in the pathogenesis of infections with coronaviruses

Frontiers in Microbiology, Journal Year: 2023, Volume and Issue: 13

Published: Jan. 13, 2023

Coronaviruses can cause serious respiratory tract infections and may also impact other end organs such as the central nervous system, lung heart. The coronavirus disease 2019 (COVID-19) has had a devastating on humanity. Understanding mechanisms that contribute to pathogenesis of infections, will set foundation for development new treatments attenuate with coronaviruses host cells tissues. During infection cells, trigger an imbalance between increased production reactive oxygen species (ROS) reduced antioxidant responses leads redox stress. Subsequently, stress contributes antiviral virus-induced inflammation apoptosis ultimately drive cell tissue damage organ disease. However, there is limited understanding how different including SARS-CoV-2, manipulate cellular machinery drives responses. This review aims elucidate involved in replication associated inflammation, apoptotic pathways, autoimmunity, vascular dysfunction collectively multiorgan damage.

Language: Английский

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