Epidemiologic Features of Recovery From SARS-CoV-2 Infection

JAMA Network Open, Journal Year: 2024, Volume and Issue: 7(6), P. e2417440 - e2417440

Published: June 17, 2024

Importance Persistent symptoms and disability following SARS-CoV-2 infection, known as post–COVID-19 condition or “long COVID,” are frequently reported pose a substantial personal societal burden. Objective To determine time to recovery infection identify factors associated with by 90 days. Design, Setting, Participants For this prospective cohort study, standardized ascertainment of was conducted starting in April 1, 2020, across 14 ongoing National Institutes Health–funded cohorts that have enrolled followed participants since 1971. This report includes data collected through February 28, 2023, on adults aged 18 years older self-reported infection. Exposure Preinfection health conditions lifestyle assessed before during the pandemic via prepandemic examinations pandemic-era questionnaires. Main Outcomes Measures Probability nonrecovery days restricted mean times were estimated using Kaplan-Meier curves, Cox proportional hazards regression performed assess multivariable-adjusted associations Results Of 4708 (mean [SD] age, 61.3 [13.8] years; 2952 women [62.7%]), an 22.5% (95% CI, 21.2%-23.7%) did not recover post Median (IQR) 20 (8-75) By there significant differences according sociodemographic, clinical, characteristics, particularly acute severity (outpatient vs critical hospitalization, 32.9 [95% 31.9-33.9 days] 57.6 51.9-63.3 days]; log-rank P < .001). Recovery vaccination prior (hazard ratio [HR], 1.30; 95% 1.11-1.51) sixth (Omicron variant) first wave (HR, 1.25; 1.06-1.49). These mediated reduced (33.4% 17.6%, respectively). unfavorably female sex 0.85; 0.79-0.92) clinical cardiovascular disease 0.84; 0.71-0.99). No observed for educational attainment, smoking history, obesity, diabetes, chronic kidney disease, asthma, obstructive pulmonary elevated depressive symptoms. similar reinfections. Conclusions Relevance In more than 1 5 within 3 months less likely those preexisting COVID-19 Omicron variant wave.

Language: Английский

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SARS-CoV-2 and the spike protein in endotheliopathy

Trends in Microbiology, Journal Year: 2023, Volume and Issue: 32(1), P. 53 - 67

Published: June 12, 2023

Language: Английский

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COVID-19-associated monocytic encephalitis (CAME): histological and proteomic evidence from autopsy

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

Published: Jan. 6, 2023

Severe neurological symptoms are associated with Coronavirus disease 2019 (COVID-19). However, the morphologic features, pathological nature and their potential mechanisms in patient brains have not been revealed despite evidence of neurotropic infection. In this study, neuropathological damages infiltrating inflammatory cells were quantitatively evaluated by immunohistochemical staining, ultrastructural examination under electron microscopy, an image threshold method, postmortem from nine critically ill COVID-19 patients age-matched cadavers healthy individuals. Differentially expressed proteins identified quantitative proteomic assays. Histopathological findings included neurophagocytosis, microglia nodules, satellite phenomena, extensive edema, focal hemorrhage, infarction, as well mononuclear cells. Immunostaining activation both astrocytes, severe damage blood-brain barrier (BBB) various degrees perivascular infiltration predominantly CD14+/CD16+/CD141+/CCR7+/CD11c+ monocytes occasionally CD4+/CD8+ T lymphocytes. Quantitative assays combined bioinformatics analysis upregulated involved immune responses, autophagy cellular metabolism compared control brains. Proteins brain development, neuroprotection, extracellular matrix basement membrane downregulated, potentially caused transforming growth factor β receptor vascular endothelial signaling pathways. Thus, our results define histopathological molecular profiles COVID-19-associated monocytic encephalitis (CAME) suggest therapeutic targets.

Language: Английский

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Long COVID-19 Pathophysiology: What Do We Know So Far?

Microorganisms, Journal Year: 2023, Volume and Issue: 11(10), P. 2458 - 2458

Published: Sept. 30, 2023

Long COVID-19 is a recognized entity that affects millions of people worldwide. Its broad clinical symptoms include thrombotic events, brain fog, myocarditis, shortness breath, fatigue, muscle pains, and others. Due to the binding virus with ACE-2 receptors, expressed in many organs, it can potentially affect any system; however, most often cardiovascular, central nervous, respiratory, immune systems. Age, high body mass index, female sex, previous hospitalization, smoking are some its risk factors. Despite great efforts define pathophysiology, gaps remain be explained. The main mechanisms described literature involve viral persistence, hypercoagulopathy, dysregulation, autoimmunity, hyperinflammation, or combination these. exact may differ from system system, but share same pathways. This review aims describe prevalent pathophysiological pathways explaining this syndrome.

Language: Английский

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Laboratory Findings and Biomarkers in Long COVID: What Do We Know So Far? Insights into Epidemiology, Pathogenesis, Therapeutic Perspectives and Challenges

International Journal of Molecular Sciences, Journal Year: 2023, Volume and Issue: 24(13), P. 10458 - 10458

Published: June 21, 2023

Long COVID (LC) encompasses a constellation of long-term symptoms experienced by at least 10% people after the initial SARS-CoV-2 infection, and so far it has affected about 65 million people. The etiology LC remains unclear; however, many pathophysiological pathways may be involved, including viral persistence; chronic, low-grade inflammatory response; immune dysregulation defective reactivation latent viruses; autoimmunity; persistent endothelial dysfunction coagulopathy; gut dysbiosis; hormonal metabolic dysregulation; mitochondrial dysfunction; autonomic nervous system dysfunction. There are no specific tests for diagnosis LC, clinical features laboratory findings biomarkers not specifically relate to LC. Therefore, is paramount importance develop validate that can employed prediction, prognosis its therapeutic response, although this effort hampered challenges pertaining non-specific nature majority manifestations in spectrum, small sample sizes relevant studies other methodological issues. Promising candidate found some patients markers systemic inflammation, acute phase proteins, cytokines chemokines; reflecting persistence, herpesviruses endotheliopathy, coagulation fibrinolysis; microbiota alterations; diverse proteins metabolites; biomarkers; cerebrospinal fluid biomarkers. At present, there only two reviews summarizing they do cover entire umbrella current biomarkers, their link etiopathogenetic mechanisms or diagnostic work-up comprehensive manner. Herein, we aim appraise synopsize available evidence on typical classification based pathogenetic main symptomatology frame epidemiological aspects syndrome furthermore assess limitations as well potential implications interventions.

Language: Английский

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Endotheliopathy in Acute COVID-19 and Long COVID

International Journal of Molecular Sciences, Journal Year: 2023, Volume and Issue: 24(9), P. 8237 - 8237

Published: May 4, 2023

The pulmonary endothelium is a highly regulated organ that performs wide range of functions under physiological and pathological conditions. Since endothelial dysfunction has been demonstrated to play direct role in sepsis acute respiratory distress syndrome, its COVID-19 also extensively investigated. Indeed, apart from the COVID-19-associated coagulopathy biomarkers, new biomarkers were recognised early during pandemic, including markers cell activation or injury. We systematically searched literature up 10 March 2023 for studies examining association between long severity outcomes biomarkers.

Language: Английский

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Effect of Thromboprophylaxis on Clinical Outcomes After COVID-19 Hospitalization

Annals of Internal Medicine, Journal Year: 2023, Volume and Issue: 176(4), P. 515 - 523

Published: March 20, 2023

Background: Patients hospitalized with COVID-19 have an increased incidence of thromboembolism. The role extended thromboprophylaxis after hospital discharge is unclear. Objective: To determine whether anticoagulation superior to placebo in reducing death and thromboembolic complications among patients discharged hospitalization. Design: Prospective, randomized, double-blind, placebo-controlled clinical trial. (ClinicalTrials.gov: NCT04650087) Setting: Done during 2021 2022 127 U.S. hospitals. Participants: Adults aged 18 years or older for 48 hours more ready discharge, excluding those a requirement for, contraindication to, anticoagulation. Intervention: 2.5 mg apixaban versus twice daily 30 days. Measurements: primary efficacy end point was 30-day composite death, arterial thromboembolism, venous safety points were major bleeding clinically relevant nonmajor bleeding. Results: Enrollment terminated early, 1217 participants randomly assigned, because lower than anticipated event rate declining hospitalizations. Median age 54 years, 50.4% women, 26.5% Black, 16.7% Hispanic; 30.7% had World Health Organization severity score 5 greater, 11.0% International Medical Prevention Registry on Venous Thromboembolism risk prediction greater 4. Incidence the 2.13% (95% CI, 1.14 3.62) group 2.31% (CI, 1.27 3.84) group. Major occurred 2 (0.4%) 1 (0.2%) 3 (0.6%) 6 (1.1%) apixaban-treated placebo-treated participants, respectively. By day 30, thirty-six (3.0%) lost follow-up, 8.5% 11.9% permanently discontinued study drug treatment. Limitations: introduction SARS-CoV-2 vaccines decreased hospitalization death. Study enrollment spanned peaks Delta Omicron variants United States, which influenced illness severity. Conclusion: thromboembolism low this cohort COVID-19. Because early termination, results imprecise inconclusive. Primary Funding Source: National Institutes Health.

Language: Английский

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COVID-19 and Long COVID: Disruption of the Neurovascular Unit, Blood-Brain Barrier, and Tight Junctions

The Neuroscientist, Journal Year: 2023, Volume and Issue: 30(4), P. 421 - 439

Published: Sept. 11, 2023

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of disease 2019 (COVID-19), could affect brain structure and function. SARS-CoV-2 can enter through different routes, including olfactory, trigeminal, vagus nerves, blood immunocytes. may also from peripheral a disrupted blood-brain barrier (BBB). The neurovascular unit in brain, composed neurons, astrocytes, endothelial cells, pericytes, protects parenchyma by regulating entry substances blood. astrocytes highly express angiotensin converting enzyme (ACE2), indicating that BBB be disturbed lead to derangements tight junction adherens proteins. This leads increased permeability, leakage components, movement immune cells into parenchyma. cross microvascular an ACE2 receptor–associated pathway. exact mechanism dysregulation COVID-19/neuro-COVID is not clearly known, nor development long COVID. Various biomarkers indicate severity neurologic complications COVID-19 help objectively diagnose those developing review highlights importance disruption, as well some potentially useful COVID-19, COVID/neuro-COVID.

Language: Английский

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Beyond Acute COVID-19: A Review of Long-term Cardiovascular Outcomes

Canadian Journal of Cardiology, Journal Year: 2023, Volume and Issue: 39(6), P. 726 - 740

Published: Feb. 6, 2023

Statistics Canada estimated that approximately 1.4 million Canadians suffer from long COVID. Although cardiovascular changes during acute SARS-CoV-2 infection are well documented, long-term sequelae less understood. In this review, we sought to characterize adult outcomes in the months after COVID-19 illness. our search identified reports of including cardiac dysautonomia, myocarditis, ischemic injuries, and ventricular dysfunction. Even patients without overt outcomes, subclinical have been observed. Cardiovascular can stem exacerbation preexisting conditions, ongoing inflammation, or as a result damage occurred infection. For example, myocardial fibrosis has reported hospital admission for illness, might be consequence myocarditis injury disease. turn, contribute further dysrhythmias heart failure. Severity risk factor consequences, however, also young, healthy individuals who had asymptomatic mild evolving evidence suggests previous disease, there is heterogeneity existing evidence, some studies marred by measured unmeasured confounders. Many investigations limited relatively short follow-up. Future should focus on longer term (beyond 1 year) identifying prevalence different populations basis COVID disease severity.

Language: Английский

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Potential of Nano-Antioxidants and Nanomedicine for Recovery from Neurological Disorders Linked to Long COVID Syndrome

Antioxidants, Journal Year: 2023, Volume and Issue: 12(2), P. 393 - 393

Published: Feb. 6, 2023

Long-term neurological complications, persisting in patients who cannot fully recover several months after severe SARS-CoV-2 coronavirus infection, are referred to as sequelae of the long COVID syndrome. Among numerous clinical post-acute COVID-19 symptoms, and psychiatric manifestations comprise prolonged fatigue, "brain fog", memory deficits, headache, ageusia, anosmia, myalgias, cognitive impairments, anxiety, depression lasting months. Considering that neurons highly vulnerable inflammatory oxidative stress damages following overproduction reactive oxygen species (ROS), neuroinflammation have been suggested dominate pathophysiological mechanisms It is emphasized mitochondrial dysfunction crucial for pathogenesis neurodegenerative disorders. Importantly, antioxidant therapies potential slow down prevent disease progression. However, many compounds display low bioavailability, instability, transport targeted tissues, limiting their applications. Various nanocarrier types, e.g., liposomes, cubosomes, solid lipid nanoparticles, micelles, dendrimers, carbon-based nanostructures, nanoceria, other inorganic can be employed enhance bioavailability. Here, we highlight phytochemical antioxidants neuroprotective agents (curcumin, quercetin, vitamins C, E D, melatonin, rosmarinic acid, N-acetylcysteine, Ginkgo Biloba derivatives) therapeutic strategies neuroregeneration. A particular focus given beneficial role nanoparticle-mediated drug-delivery systems addressing challenges managing preventing disorders factors sequelae.

Language: Английский

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