The laboratory parameters in predicting the severity and death of COVID-19 patients: Future pandemic readiness strategies DOI Creative Commons
Ahmad R. Alsayed, Syed Imran Ahmed,

Anas Osama AL Shweiki

et al.

Biomolecules and Biomedicine, Journal Year: 2023, Volume and Issue: 24(2), P. 238 - 255

Published: Sept. 14, 2023

The range of clinical manifestations associated with the infection by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) encompasses a broad spectrum, ranging from flu-like symptoms to occurrence multiple organ failure and death. severity disease 2019 (COVID-19) is categorized based on presentation divided into three distinct levels identified as non-severe, severe, critical. Although individuals all age groups are susceptible SARS-CoV-2 infection, middle-aged older adults more frequently impacted, latter being likely develop illness. Various laboratory characteristics observed in hospitalized COVID-19 patients have been correlated adverse outcomes. These include elevated D-dimer, liver enzymes, lactate dehydrogenase, C-reactive protein, ferritin, prothrombin time, troponin, well decreased lymphocyte platelets counts. This review investigated relationship between baseline characteristics, initial parameters upon hospital admission, illness mortality rates among patients. pandemic has concluded, understanding predictors virus remains crucial, examining these can long-term effects. Such insights help healthcare systems manage resources effectively deliver timely appropriate care identifying targeting high-risk individuals. knowledge also us better prepare for future pandemics. By predictors, we take steps protect public health mitigate impact

Language: Английский

Mechanistic insights from inflammasome structures DOI
Jianing Fu, Kate Schroder, Hao Wu

et al.

Nature reviews. Immunology, Journal Year: 2024, Volume and Issue: 24(7), P. 518 - 535

Published: Feb. 19, 2024

Language: Английский

Citations

64
Induction of the Inflammasome by the SARS‐CoV‐2 Accessory Protein ORF9b, Abrogated by Small‐Molecule ORF9b Homodimerization Inhibitors DOI
Erika Zodda, Mònica Pons, Natàlia DeMoya‐Valenzuela

et al.

Journal of Medical Virology, Journal Year: 2025, Volume and Issue: 97(2)

Published: Feb. 1, 2025

ABSTRACT Viral accessory proteins play critical roles in viral escape from host innate immune responses and inflammatory pathogenesis. Here we show that the SARS‐CoV‐2 protein, ORF9b, but not other (ORF3a, ORF3b, ORF6, ORF7, ORF8, ORF9c, ORF10), strongly activates inflammasome‐dependent caspase‐1 A549 lung carcinoma cells THP‐1 monocyte‐macrophage cells. Exposure to lipopolysaccharide (LPS) ATP additively enhanced activation of by suggesting ORF9b LPS follow parallel pathways inflammasome caspase‐1. Following rational silico approaches, have designed small molecules capable inhibiting homodimerization which experimentally inhibited ORF9b‐ORF9b homotypic interactions, caused mitochondrial eviction ORF9b‐induced cells, cytokine release restored type I interferon (IFN‐I) signaling suppressed both cell models. These are first‐in‐class compounds targeting a protein for viral‐induced exacerbated inflammation responses, with potential mitigating severe immunopathogenic damage induced highly pathogenic coronaviruses restoring antiviral curtailed infection.

Language: Английский

Citations

1
Immunologic and inflammatory consequences of SARS-CoV-2 infection and its implications in renal disease DOI Creative Commons

Hiam Naiditch,

Michael R. Betts,

H. Benjamin Larman

et al.

Frontiers 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

1
Host mitochondria: more than an organelle in SARS-CoV-2 infection DOI Creative Commons
Shahrzad Shoraka, Amali E. Samarasinghe, Amir Ghaemi

et al.

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

Published: Aug. 25, 2023

Since December 2019, the world has been facing viral pandemic called COVID-19 (Coronavirus disease 2019) caused by a new beta-coronavirus named severe acute respiratory syndrome coronavirus-2, or SARS-CoV-2. patients may present with wide range of symptoms, from asymptomatic to requiring intensive care support. The form is often marked an altered immune response and cytokine storm. Advanced age, age-related underlying diseases, including metabolic syndromes, appear contribute increased severity mortality suggesting role for mitochondria in pathogenesis. Furthermore, since system associated its damage-related molecular patterns (mtDAMPs), host mitochondrial play important during infections. Viruses have evolved modulate function survival proliferation, which turn could lead cellular stress progression. Recent studies focused on possible roles SARS-CoV-2 infection. It suggested that hijacking be key factor In this review, we discuss infections infection based past knowledge. Paying attention will help better understand pathophysiology achieve effective methods prevention, diagnosis, treatment.

Language: Английский

Citations

17
Differences and similarities between innate immune evasion strategies of human coronaviruses DOI Creative Commons
Helene Hoenigsperger, Rinu Sivarajan, Konstantin M. J. Sparrer

et al.

Current Opinion in Microbiology, Journal Year: 2024, Volume and Issue: 79, P. 102466 - 102466

Published: March 30, 2024

So far, seven coronaviruses have emerged in humans. Four recurring endemic cause mild respiratory symptoms. Infections with epidemic Middle East syndrome–related coronavirus or severe acute syndrome (SARS-CoV)-1 are associated high mortality rates. SARS-CoV-2 is the causative agent of disease 2019 pandemic. To establish an infection, evade restriction by human innate immune defenses, such as interferon system, autophagy and inflammasome. Here, we review similar distinct manipulation strategies employed coronaviruses. We further discuss impact on pathogenesis, zoonotic emergence adaptation. Understanding nature interplay between endemic/epidemic/pandemic host defenses may help to better assess pandemic potential emerging

Language: Английский

Citations

8
Exploring the Pathophysiology of Long COVID: The Central Role of Low-Grade Inflammation and Multisystem Involvement DOI Open Access
Evgeni Gusev, Alexey Sarapultsev

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(12), P. 6389 - 6389

Published: June 9, 2024

Long COVID (LC), also referred to as Post COVID-19 Condition, Post-Acute Sequelae of SARS-CoV-2 Infection (PASC), and other terms, represents a complex multisystem disease persisting after the acute phase COVID-19. Characterized by myriad symptoms across different organ systems, LC presents significant diagnostic management challenges. Central disorder is role low-grade inflammation, non-classical inflammatory response that contributes chronicity diversity observed. This review explores pathophysiological underpinnings LC, emphasizing importance inflammation core component. By delineating pathogenetic relationships clinical manifestations this article highlights necessity for an integrated approach employs both personalized medicine standardized protocols aimed at mitigating long-term consequences. The insights gained not only enhance our understanding but inform development therapeutic strategies could be applicable chronic conditions with similar features.

Language: Английский

Citations

8
Severe pediatric COVID-19: a review from the clinical and immunopathophysiological perspectives DOI Creative Commons

Yikan Sun,

Can Wang,

Peiquan Lin

et al.

World Journal of Pediatrics, Journal Year: 2024, Volume and Issue: 20(4), P. 307 - 324

Published: Feb. 6, 2024

Coronavirus disease 2019 (COVID-19) tends to have mild presentations in children. However, severe and critical cases do arise the pediatric population with debilitating systemic impacts can be fatal at times, meriting further attention from clinicians. Meanwhile, intricate interactions between pathogen virulence factors host defense mechanisms are believed play indispensable roles COVID-19 pathophysiology but remain incompletely understood.

Language: Английский

Citations

4
The entrenchment of NLRP3 inflammasomes in autoimmune disease-related inflammation DOI Creative Commons

Valeria Carnazzo,

Donato Rigante, Giuliana Restante

et al.

Autoimmunity Reviews, Journal Year: 2025, Volume and Issue: unknown, P. 103815 - 103815

Published: April 1, 2025

Autoinflammation and autoimmunity are almost "opposite" phenomena characterized by chronic activation of the immune system, 'innate' in first 'adaptive' second, leading to inflammation several tissues with specific protean effectors tissue damage. The mechanism involvement multiprotein complexes called 'inflammasomes' within autoimmune pictures, differently from autoinflammatory conditions, is yet undeciphered. In this review we provide a comprehensive overview on NLRP3 inflammasome contribution into pathogenesis some diseases. response autoantibodies against nucleic acids or tissue-specific antigens activated dendritic cells macrophages patients systemic lupus erythematosus. Crucial amplify interleukin-1 overexpression matrix metalloproteinase production at joint level rheumatoid arthritis. A deregulated occurs serous acini salivary lacrimal glands prone Sjogren's syndrome, but also inflammatory process involving endothelial cells, leucocyte recruitment, platelet plugging vasculitides. Furthermore, organ-specific diseases such as thyroiditis hepatitis may display hyperactive inflammasomes resident thyroid liver, respectively. Therefore, it not unexpected that preclinical studies have shown how inhibitors significantly overthrow severity different slow down their trend towards an ominous progression. Specific markers could reveal subclinical components escaping conventional diagnostic approaches improve monitoring personalizing treatment.

Language: Английский

Citations

0
Innate immune mechanisms of infection: what we know and potential conserved mechanisms affecting sleep during infection DOI Creative Commons

Mark R. Zielinski,

Sean D. Carey,

John A. Craig

et al.

Neurobiology of Sleep and Circadian Rhythms, Journal Year: 2025, Volume and Issue: unknown, P. 100121 - 100121

Published: April 1, 2025

Language: Английский

Citations

0
Beyond acute infection: molecular mechanisms underpinning cardiovascular complications in long COVID DOI Creative Commons

Roba Hamed Mostafa,

Ahmed A. Moustafa

Frontiers in Cardiovascular Medicine, Journal Year: 2024, Volume and Issue: 11

Published: Feb. 14, 2024

SARS-CoV-2, responsible for the global COVID-19 pandemic, has manifested significant cardiovascular implications infected population. These repercussions not only linger beyond initial phase of illness but have also been observed in individuals who remain asymptomatic. This extended and pervasive impact is often called post-acute syndrome (PACS) or “Long COVID”. With number confirmed cases approaching an alarming 756 million, multifaceted challenges Long COVID are undeniable. span from individual health complications to considerable burdens on worldwide healthcare systems. Our review comprehensively examines persistent associated with COVID-19. Furthermore, we shed light emerging therapeutic strategies that promise manage possibly mitigate these complications. We introduce discuss profound concerns regarding potential transgenerational emphasizing need a proactive informed approach future research clinical practice.

Language: Английский

Citations

3