Immunopathogenesis and Immunogenetic Variants in COVID-19 DOI
Pakorn Sagulkoo, Kitiporn Plaimas, Apichat Suratanee

et al.

Current Pharmaceutical Design, Journal Year: 2022, Volume and Issue: 28(22), P. 1780 - 1797

Published: May 22, 2022

Coronavirus disease 2019 (COVID-19) continues to spread globally despite the discovery of vaccines. Many people die due COVID-19 as a result catastrophic consequences, such acute respiratory distress syndrome, pulmonary embolism, and disseminated intravascular coagulation caused by cytokine storm. Immunopathology immunogenetic research may assist in diagnosing, predicting, treating severe storm associated with COVID-19. This paper reviews immunopathogenesis variants that play role Although various immune-related genetic have been investigated relation COVID-19, NOD-like receptor protein 3 (NLRP3) interleukin 18 (IL-18) not assessed for their potential significance clinical outcome. Here, we a) summarize current understanding etiology pathophysiology storm; b) construct analyze protein-protein interaction (PPI) networks (using enrichment annotation analysis) based on NLRP3 IL18 all genes, which were established Our PPI network analyses predict useful drug targets prevent onset including key antiviral pathways Toll-Like-Receptor cascades, signaling, RIG-induction interferon (IFN) α/β, (IL)-1, IL-6, IL-12, IL-18, tumor necrosis factor signaling; SARS-CoV-2 innate immune evasion participation MYD88 MAVS The be used more outcomes, thereby opening door targeted preventive treatments.

Language: Английский

The roles of critical pro‐inflammatory cytokines in the drive of cytokine storm during SARS‐CoV‐2 infection DOI Creative Commons
Muhammad Suhaib Qudus, Mingfu Tian,

Summan Sirajuddin

et al.

Journal of Medical Virology, Journal Year: 2023, Volume and Issue: 95(4)

Published: April 1, 2023

Abstract In patients with severe COVID‐19, acute respiratory distress syndrome (ARDS), multiple organ dysfunction (MODS), and even mortality can result from cytokine storm, which is a hyperinflammatory medical condition caused by the excessive uncontrolled release of pro‐inflammatory cytokines. High levels numerous crucial cytokines, such as interleukin‐1 (IL‐1), IL‐2, IL‐6, tumor necrosis factor‐α, interferon (IFN)‐γ, IFN‐induced protein 10 kDa, granulocyte‐macrophage colony‐stimulating factor, monocyte chemoattractant protein‐1, IL‐10 so on, have been found in COVID‐19. They participate cascade amplification pathways responses through complex inflammatory networks. Here, we review involvements these critical cytokines SARS‐CoV‐2 infection discuss their potential roles triggering or regulating help to understand pathogenesis So far, there rarely effective therapeutic strategy for storm besides using glucocorticoids, proved fatal side effects. Clarifying key involved network will develop an ideal intervention, neutralizing antibody certain inhibitor some signal pathways.

Language: Английский

Citations

50

Covid-19 a triggering factor of autoimmune and multi-inflammatory diseases DOI Creative Commons

Emina Karahmet Sher,

Adnan Ćosović,

Amina Džidić-Krivić

et al.

Life Sciences, Journal Year: 2023, Volume and Issue: 319, P. 121531 - 121531

Published: Feb. 27, 2023

SARS-CoV-2 virus has attracted a lot of attention globally due to the autoimmune and inflammatory processes that were observed during development Covid-19 disease. Excessive activation immune response triggering autoantibodies synthesis as well an excessive cytokines onset cytokine storm vital role in disease outcome occurring complications. This scenario is reminiscent infiltration lymphocytes monocytes specific organs increased production chemoattractants noted other diseases. The main goal this study investigate complex occur find similarities with diseases such multiple sclerosis (MS), acute respiratory distress syndrome (ARDS), rheumatoid arthritis (RA) Kawasaki advance existing diagnostic therapeutic protocols. therapy Interferon-gamma (IFN-γ) use S1P receptor modulators showed promising results. However, there are many unknowns about these mechanisms possible novel therapies. Therefore, inflammation autoimmunity triggered by should be further investigated improve procedures protocols for Covid-19.

Language: Английский

Citations

45

Pathophysiological, immunological, and inflammatory features of long COVID DOI Creative Commons
Karen Böhmwald, Benjamín Diethelm‐Varela,

Linmar Rodríguez-Guilarte

et al.

Frontiers in Immunology, Journal Year: 2024, Volume and Issue: 15

Published: Feb. 28, 2024

The COVID-19 pandemic continues to cause severe global disruption, resulting in significant excess mortality, overwhelming healthcare systems, and imposing substantial social economic burdens on nations. While most of the attention therapeutic efforts have concentrated acute phase disease, a notable proportion survivors experience persistent symptoms post-infection clearance. This diverse set symptoms, loosely categorized as long COVID, presents potential additional public health crisis. It is estimated that 1 5 exhibit clinical manifestations consistent with COVID. Despite this prevalence, mechanisms pathophysiology COVID remain poorly understood. Alarmingly, evidence suggests cases within condition develop debilitating or disabling symptoms. Hence, urgent priority should be given further studies equip systems for its management. review provides an overview available information emerging condition, focusing affected individuals’ epidemiology, pathophysiological mechanisms, immunological inflammatory profiles.

Language: Английский

Citations

20

COVID-19 Mechanisms in the Human Body—What We Know So Far DOI Creative Commons
Ashutosh Kumar, Ravi Kant Narayan, Pranav Prasoon

et al.

Frontiers in Immunology, Journal Year: 2021, Volume and Issue: 12

Published: Nov. 1, 2021

More than one and a half years have elapsed since the commencement of coronavirus disease 2019 (COVID-19) pandemic, world is struggling to contain it. Being caused by previously unknown virus, in initial period, there had been an extreme paucity knowledge about mechanisms, which hampered preventive therapeutic measures against COVID-19. In endeavor understand pathogenic extensive experimental studies conducted across globe involving cell culture-based experiments, human tissue organoids, animal models, targeted various aspects disease, viz., viral properties, tropism organ-specific pathogenesis, involvement physiological systems, immune response infection. The vastly accumulated scientific on all COVID-19 has currently changed scenario from great despair hope. Even though spectacular progress made these aspects, multiple gaps are remaining that need be addressed future studies. Moreover, severe acute respiratory syndrome 2 (SARS-CoV-2) variants emerged onset first wave, with seemingly greater transmissibility/virulence escape capabilities wild-type strain. this review, we narrate pandemic regarding mechanisms body, including virus-host interactions, pulmonary other systemic manifestations, immunological dysregulations, complications, host-specific vulnerability, long-term health consequences survivors. Additionally, provide brief review current evidence explaining molecular imparting transmissibility virulence emerging SARS-CoV-2 variants.

Language: Английский

Citations

64

A review of Covid-19 and acute kidney injury: from pathophysiology to clinical results DOI Creative Commons
Inah Maria Drummond Pecly, Rafael Bellotti Azevedo, Elizabeth Silaid Muxfeldt

et al.

Brazilian Journal of Nephrology, Journal Year: 2021, Volume and Issue: 43(4), P. 551 - 571

Published: May 28, 2021

Abstract Acute kidney injury (AKI) in hospitalized patients with COVID-19 is associated higher mortality and a worse prognosis. Nevertheless, most have mild symptoms, about 5% can develop more severe symptoms involve hypovolemia multiple organ dysfunction syndrome. In pathophysiological perspective, SARS-CoV-2 infection characterized by numerous dependent pathways triggered hypercytokinemia, especially IL-6 TNF-alpha, leading to systemic inflammation, hypercoagulability, dysfunction. Systemic endotheliitis direct viral tropism proximal renal tubular cells podocytes are important mechanisms critical infection, clinical presentation ranging from proteinuria and/or glomerular hematuria fulminant AKI requiring replacement therapies. Glomerulonephritis, rhabdomyolysis, nephrotoxic drugs also damage COVID-19. Thus, independent risk factors for infection. We provide comprehensive review of the literature emphasizing impact acute involvement evolutive prognosis

Language: Английский

Citations

57

The mechanism of multiple organ dysfunction syndrome in patients with COVID‐19 DOI

Wenbin Zhao,

Hanmeng Li,

Jianghua Li

et al.

Journal of Medical Virology, Journal Year: 2022, Volume and Issue: 94(5), P. 1886 - 1892

Published: Jan. 28, 2022

In late 2019, an outbreak of coronavirus disease 2019 (COVID-19) arose, caused by severe acute respiratory syndrome type 2 (SARS-CoV-2). This rapidly became a public health event international concern. addition to the most typical symptoms dyspnea, numerous patients with COVID-19 exhibited systemic symptoms, such as cardiovascular disease, liver and kidney failure, disorders in coagulation. At present, clinical data indicates that who are critically ill die from multiple organ dysfunction syndromes (MODS). Moreover, entry SARS-CoV-2 into cells causing pathology progressive failure is precisely mediated human angiotensin-converting enzyme protein. plays role maintaining both fluid electrolyte homeostasis, ensuring stability internal environment. Therefore, present review aimed investigate pathogenesis MODS infection based on current previous studies.

Language: Английский

Citations

51

Mechanisms of COVID-19-induced kidney injury and current pharmacotherapies DOI Creative Commons
Wissam H. Faour,

Ali Choaib,

Elio Issa

et al.

Inflammation Research, Journal Year: 2021, Volume and Issue: 71(1), P. 39 - 56

Published: Nov. 21, 2021

The COVID-19 pandemic created a worldwide debilitating health crisis with the entire humanity suffering from deleterious effects associated high infectivity and mortality rates. While significant evidence is currently available online targets various aspects of disease, both inflammatory noninflammatory kidney manifestations secondary to infection are still largely underrepresented. In this review, we summarized current knowledge about COVID-19-related manifestations, their pathologic mechanisms as well pharmacotherapies used treat patients COVID-19. We also shed light on effect these medications functions that can further enhance renal damage illness.

Language: Английский

Citations

51

Evidence for SARS-CoV-2 Spike Protein in the Urine of COVID-19 Patients DOI Creative Commons
Santosh George, Anasuya Pal, J. Gagnon

et al.

Kidney360, Journal Year: 2021, Volume and Issue: 2(6), P. 924 - 936

Published: April 14, 2021

Abstract Key Points Using an antigen capture assay to detect severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike S1 protein, we found that the protein is present in urine of 25% patients with disease 2019 (COVID-19). Further, 24% and 21% adult COVID-19 have high levels albumin cystatin C, respectively. The presence SARS-CoV-2 suggests renal abnormalities resulting from COVID-19. Background infection has, as April 2021, affected >133 million people worldwide, causing >2.5 deaths. Because large majority individuals infected are asymptomatic, major concerns been raised about possible long-term consequences infection. Methods Wedeveloped samples COVID-19whose diagnosis was confirmed by positive PCR results nasopharyngeal swabs (NP-PCR+) forSARS-CoV-2. We used a collection 233 132 participants Yale New Haven Hospital Children’s Philadelphia were obtained during pandemic (106 NP-PCR+ 26 NP-PCR−), 20 collected before pandemic. Results Our analysis identified 23 out 91 (25%) (Ur-S+). Interestingly, although all children Ur-S−, one child who NP-PCR− be for their urine. Of adults Ur-S+, only individual showed detectable viral RNA further had respectively, Among albuminuria (>0.3 mg/mg creatinine), statistical correlation could between Conclusions Together, our data four develop abnormalities, such albuminuria. Awareness effect these findings warranted.

Language: Английский

Citations

48

Coronavirus disease-19: The multi-level, multi-faceted vasculopathy DOI Creative Commons
Thiago Quinaglia, Mahsima Shabani, Íkaro Breder

et al.

Atherosclerosis, Journal Year: 2021, Volume and Issue: 322, P. 39 - 50

Published: Feb. 15, 2021

The new coronavirus disease (COVID-19) is a systemic disease. Mounting evidence depict signs and symptoms involving multiple organs, most of which supported by pathological data. A plausible link to these manifestations vascular endothelial dysfunction/damage. However, much the current knowledge relies on opinion incipient evidence. We aim objectively appraise association between COVID-19 disease, specifically endotheliitis vasculitis.

Language: Английский

Citations

45

Longitudinal prediction of hospital-acquired acute kidney injury in COVID-19: a two-center study DOI Creative Commons
Justin Y. Lu, Wei Hou, Timothy Q. Duong

et al.

Infection, Journal Year: 2021, Volume and Issue: 50(1), P. 109 - 119

Published: June 26, 2021

Language: Английский

Citations

43