
Informatics in Medicine Unlocked, Journal Year: 2025, Volume and Issue: unknown, P. 101649 - 101649
Published: May 1, 2025
Language: Английский
Informatics in Medicine Unlocked, Journal Year: 2025, Volume and Issue: unknown, P. 101649 - 101649
Published: May 1, 2025
Language: Английский
eLife, Journal Year: 2023, Volume and Issue: 12
Published: March 22, 2023
COVID-19, with persistent and new onset of symptoms such as fatigue, post-exertional malaise, cognitive dysfunction that last for months impact everyday functioning, is referred to Long COVID under the general category post-acute sequelae SARS-CoV-2 infection (PASC). PASC highly heterogenous may be associated multisystem tissue damage/dysfunction including acute encephalitis, cardiopulmonary syndromes, fibrosis, hepatobiliary damages, gastrointestinal dysregulation, myocardial infarction, neuromuscular neuropsychiatric disorders, pulmonary damage, renal failure, stroke, vascular endothelial dysregulation. A better understanding pathophysiologic mechanisms underlying essential guide prevention treatment. This review addresses potential hypotheses connect long-term health consequences. Comparisons between other virus-initiated chronic syndromes myalgic encephalomyelitis/chronic fatigue syndrome postural orthostatic tachycardia will addressed. Aligning identifying potentially regulated common underlining pathways necessary true nature PASC. The discussed contributors include from injury one or more organs, reservoirs replicating virus its remnants in several tissues, re-activation latent pathogens Epstein-Barr herpes viruses COVID-19 immune-dysregulated environment, interactions host microbiome/virome communities, clotting/coagulation dysfunctional brainstem/vagus nerve signaling, dysautonomia autonomic dysfunction, ongoing activity primed immune cells, autoimmunity due molecular mimicry pathogen proteins. individualized suggests different therapeutic approaches required best manage specific patients.
Language: Английский
Citations
152Bosnian Journal of Basic Medical Sciences, Journal Year: 2022, Volume and Issue: unknown
Published: Sept. 16, 2022
The SARS-CoV-2 infection causes COVID-19, which has affected approximately six hundred million people globally as of August 2022. Organs and cells harboring angiotensin-converting enzyme 2 (ACE2) surface receptors are the primary targets virus. However, once it enters body through respiratory system, virus can spread hematogenously to infect other organs. Therefore, COVID-19 affects many organs, causing severe long-term complications, even after disease ended, thus worsening quality life. Although is known that system most by infection, organs/systems in short long term. Since simultaneously redesigning diagnostic therapy policies fit damaged organs strongly recommended. Even though pathophysiology problems unknown, frequency cases rises with age existence preexisting symptoms. This study aims update our knowledge multi-organ dysfunction interaction based on clinical theoretical evidence. For this purpose, comprehensively elucidates recent studies effects multiple systems, including respiratory, cardiovascular, gastrointestinal, renal, nervous, endocrine, reproductive, immune, parts integumentary system. Understanding range atypical symptoms could improve surveillance, limit transmission, avoid additional multi-organ-system problems.
Language: Английский
Citations
70Nature Reviews Endocrinology, Journal Year: 2024, Volume and Issue: 20(6), P. 336 - 348
Published: Feb. 12, 2024
Language: Английский
Citations
18International Journal of Molecular Sciences, Journal Year: 2022, Volume and Issue: 23(13), P. 7326 - 7326
Published: June 30, 2022
Coronavirus disease 2019 (COVID-19) is a highly heterogeneous regarding severity, vulnerability to infection due comorbidities, and treatment approaches. The hypothalamic-pituitary-adrenal (HPA) axis has been identified as one of the most critical endocrine targets severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that might significantly impact outcomes after infection. Herein we review rationale for glucocorticoid use in setting COVID-19 emphasize need have low index suspicion glucocorticoid-induced adrenal insufficiency, adjusting formulation used, dose, duration, underlying health problems. We also address several additional mechanisms may cause HPA dysfunction, including illness-related corticosteroid direct cytopathic impacts SARS-CoV-2 on adrenals, pituitary, hypothalamus, immune-mediated inflammations, small vessel vasculitis, microthrombotic events, resistance cortisol receptors, impaired post-receptor signaling, well dissociation ACTH regulation. discuss increased risk more illness patients with pre-existing disorders axis, from insufficiency excess. These insights into complex regulation reveal how body performs its adaptive survival mechanism during infection, such SARS-CoV-2, many parameters disbalance this adaptation.
Language: Английский
Citations
54Hypertension Research, Journal Year: 2022, Volume and Issue: 46(3), P. 601 - 619
Published: Dec. 27, 2022
Language: Английский
Citations
43European Journal of Human Genetics, Journal Year: 2023, Volume and Issue: 32(1), P. 10 - 20
Published: Nov. 8, 2023
Abstract COVID-19, the disease caused by SARS-CoV-2, has significant morbidity and mortality worldwide. The betacoronavirus continues to evolve with global health implications as we race learn more curb its transmission, evolution, sequelae. focus of this review, second a three-part series, is on biological effects SARS-CoV-2 virus post-acute in context tissue organ adaptations damage. We highlight current knowledge describe how virological, animal, clinical studies have shed light mechanisms driving varied diagnoses observations COVID-19 patients. Moreover, investigations into informed understanding viral pathogenesis provide innovative pathways for future research diseases.
Language: Английский
Citations
29Frontiers in Immunology, Journal Year: 2025, Volume and Issue: 15
Published: Feb. 12, 2025
The emergence of the COVID-19 pandemic made it critical to understand immune and inflammatory responses SARS-CoV-2 virus. It became increasingly recognized that response was a key mediator illness severity its mechanisms needed be better understood. Early infection both tissue cells, such as macrophages, leading pyroptosis-mediated inflammasome production in an organ system for systemic oxygenation likely plays central role morbidity wrought by SARS-CoV-2. Delayed transcription Type I III interferons may lead early disinhibition viral replication. Cytokines interleukin-1 (IL-1), IL-6, IL-12, tumor necrosis factor α (TNFα), some which produced through involving nuclear kappa B (NF-κB), contribute hyperinflammatory state patients with severe COVID-19. Lymphopenia, more apparent among natural killer (NK) CD8+ T-cells, B-cells, can disease reflect direct cytopathic effects or end-organ sequestration. Direct activation endothelial cells mechanism systems are impacted. In this context, endovascular neutrophil extracellular trap (NET) formation microthrombi development seen lungs other organs throughout body, heart, gut, brain. kidney most impacted extrapulmonary owing high concentration ACE2 exposure kidney, acute tubular injury, myofibroblast activation, collapsing glomerulopathy select populations account COVID-19-related AKI CKD development. COVID-19-associated nephropathy (COVAN), particular, mediated IL-6 signal transducer activator 3 (STAT3) signaling, suggesting connection between chronic disease. Chronic manifestations also include conditions like Multisystem Inflammatory Syndrome Children (MIS-C) Adults (MIS-A) post-acute sequelae (PASC), spectrum clinical presentations persistent dysregulation. lessons learned those undergoing continued study have broad implications understanding infections’ immunologic consequences beyond coronaviruses.
Language: Английский
Citations
1Prion, Journal Year: 2023, Volume and Issue: 17(1), P. 82 - 104
Published: March 30, 2023
The crosstalk between viral infections, amyloid formation and neurodegeneration has been discussed with varying intensity since the last century. Several proteins are known to be amyloidogenic. Post-acute sequalae (PAS) of infections is for several viruses. SARS-CoV-2 COVID-19 implicate connections severe outcomes in acute infection, PAS neurodegenerative diseases. Is connection causation or just correlation? In this review we highlight aspects where amyloids viruses meet. evolutionary driving forces that dictate protein propensity different compared prokaryotes eukaryotes, while posttranslational endoproteolysis appears a common mechanism leading up both human proteins. Not only do form irrespective each other but there also examples co-operativity amyloids, inter-, intra-host spread respective entity. Abnormal blood clotting long COVID as side effect some vaccine recipients connected fibrin Spike-protein. We conclude many intersects and, consequently, virus research need join here. emphasize accelerate development implementation clinical practice antiviral drugs preclude downstream neurological damage. There an ample retake on suitable antigen targets further next generation vaccines against current coming pandemics.
Language: Английский
Citations
20Best Practice & Research Clinical Endocrinology & Metabolism, Journal Year: 2023, Volume and Issue: 37(4), P. 101752 - 101752
Published: Feb. 27, 2023
Language: Английский
Citations
17Reviews in Endocrine and Metabolic Disorders, Journal Year: 2024, Volume and Issue: unknown
Published: Oct. 7, 2024
Abstract GHRH is a neuropeptide associated with diverse variety of activities in human physiology and immune responses. The present study reviews the latest information on involvement system inflammation, suggesting that antagonists may deliver new therapeutic possibility disorders related to dysfunction inflammation.
Language: Английский
Citations
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