CyHV-2 infection triggers mitochondrial-mediated apoptosis in GiCF cells by upregulating the pro-apoptotic gene ccBAX

Fish & Shellfish Immunology, Journal Year: 2024, Volume and Issue: 147, P. 109400 - 109400

Published: Jan. 20, 2024

Language: Английский

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Host Subcellular Organelles: Targets of Viral Manipulation

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(3), P. 1638 - 1638

Published: Jan. 29, 2024

Viruses have evolved sophisticated mechanisms to manipulate host cell processes and utilize intracellular organelles facilitate their replication. These complex interactions between viruses cellular allow them hijack the machinery impair homeostasis. Moreover, viral infection alters membrane’s structure composition induces vesicle formation trafficking of components. However, research focus has predominantly been on immune response elicited by viruses, often overlooking significant alterations that induce in organelles. Gaining a deeper understanding these virus-induced changes is crucial for elucidating full life cycle developing potent antiviral therapies. Exploring could substantially improve our mechanisms.

Language: Английский

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Mechanism of Nanoparticle Toxicity

Published: Jan. 1, 2024

Nanoparticles (NPs), materials less than 100 nm in size, are being utilised diverse biomedical, commercial, and industrial applications due to their unique physicochemical properties. However, the same properties that make nanoparticles so appealing for novel uses also raise concerns regarding potential health environmental impacts. A significant body of vitro vivo research over past two decades has aimed elucidate mechanisms by which induce adverse effects. Nanoparticle toxicity is mediated through a multifaceted process encompassing interactions with biological components at molecular, cellular, tissue levels. Oxidative stress, inflammation, physical disruption cell membranes, alteration signalling pathways have been identified as key events induced organisms. can penetrate into cells stimulate excessive reactive oxygen species formation damages lipids, proteins, DNA. They trigger inflammatory responses activation cascades molecular mediators. Cationic directly interact damage membranes. Biodistribution accumulation organs time lead chronic inflammation. Soluble nanoparticle like metal ions drive oxidative damage, protein binding, enzyme inhibition, other mechanisms. Other factors influencing include surface adsorption dissolution, aggregation state, ability cross barriers. comprehensive understanding critical appropriate safety assessment design nanomaterials.

Language: Английский

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Taurolithocholic acid protects against viral haemorrhagic fever via inhibition of ferroptosis

Nature Microbiology, Journal Year: 2024, Volume and Issue: unknown

Published: Sept. 18, 2024

Language: Английский

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Inhibition of PERK Kinase, an Orchestrator of the Unfolded Protein Response (UPR), Significantly Reduces Apoptosis and Inflammation of Lung Epithelial Cells Triggered by SARS-CoV-2 ORF3a Protein

Biomedicines, Journal Year: 2023, Volume and Issue: 11(6), P. 1585 - 1585

Published: May 30, 2023

SARS-CoV-2 ORF3a accessory protein was found to be involved in virus release, immunomodulation and exhibited a pro-apoptotic character. In order unravel potential ORF3a-induced apoptotic inflammatory death mechanism, lung epithelial cells (A549) were transfected with vitro synthesized mRNA. The protein's dynamic involvement as "stress factor" for the endoplasmic reticulum, causing activation of PERK kinase other UPR-involved proteins therefore upregulation their signaling pathway executioners (ATF6, XBP-1s, PERK, phospho eIF2a, ATF4, CHOP, GADD34), has been clearly demonstrated. Furthermore, overexpression BAX BH3-only PUMA, Bcl-2 family genes (BAX, BAK, BID, BAD), reduced expression mRNA levels, lastly, cleavage PARP-1 caspase members (caspase-3,-8 -9) indicate that displays its character through mitochondrial apoptosis. Moreover, NFκB, phosphorylation p65 IκΒα elevated pro-inflammatory cytokines (IL-1b, IL-6, IL-8 IL-18) this causes response NFκB triggers injury. An intriguing finding our study is upon treatment ORF3a-transfected GSK2606414, selective inhibitor, both complications (apoptosis response) neutralized, cell survival favored, whereas z-VAD (a pan-caspase inhibitor) despite inhibiting death, could not ameliorate A549 cells. Given above, we point out "master tactician" constitutes main stimulus emergence nature serve target developing novel therapeutic approaches against COVID-19.

Language: Английский

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Unveiling the intersection: ferroptosis in influenza virus infection

Virology Journal, Journal Year: 2024, Volume and Issue: 21(1)

Published: Aug. 12, 2024

The influenza virus (IFV) imposes a considerable health and economic burden globally, requiring comprehensive understanding of its pathogenic mechanisms. Ferroptosis, an iron-dependent lipid peroxidation cell death pathway, holds unique implications for the antioxidant defense system, with possible contributions to inflammation. This exploration focuses on dynamic interplay between ferroptosis host against viruses, emphasizing influence IFV infections activation pathway. causes different types death, including apoptosis, necrosis, ferroptosis. IFV-induced ferroptotic is mediated by alterations in iron homeostasis, intensifying accumulation reactive oxygen species promoting peroxidation. A investigation into mechanism viral infections, specifically IFV, has great potential identify therapeutic strategies. may pave way development drugs using inhibitors, presenting effective approach suppress infections.

Language: Английский

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The Diagnostic, Prognostic, and Therapeutic Potential of Cell-Free DNA with a Special Focus on COVID-19 and Other Viral Infections

International Journal of Molecular Sciences, Journal Year: 2023, Volume and Issue: 24(18), P. 14163 - 14163

Published: Sept. 15, 2023

Cell-free DNA (cfDNA) in human blood serum, urine, and other body fluids recently became a commonly used diagnostic marker associated with various pathologies. This is because cfDNA enables much higher sensitivity than standard biochemical parameters. The presence of and/or increased level has been reported for diseases, including viral infections, COVID-19. Here, we review general, how it identified, where can derive from, its molecular features, mechanisms release clearance. General suitability questions, possible shortcomings future directions are discussed, special focus on coronavirus infection.

Language: Английский

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The role of pyroptosis in viral infection

Archives of Virology, Journal Year: 2024, Volume and Issue: 169(3)

Published: March 1, 2024

Language: Английский

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Orthogonal Persulfide Generation through Precision Tools Provides Insights into Mitochondrial Sulfane Sulfur

Angewandte Chemie, Journal Year: 2024, Volume and Issue: 136(46)

Published: Aug. 2, 2024

Abstract The sulfane sulfur pool, comprised of persulfide (RS‐SH) and polysulfide (RS‐S n H) derived from hydrogen sulfide (H 2 S), has emerged as a major player in redox biochemistry. Mitochondria, besides energy generation, serve significant cellular hubs, mediate stress response health. However, the effects endogenous mitochondrial (MSS) remain largely uncharacterized compared with their cytosolic counterparts, (CSS). To investigate this, we designed novel artificial substrate for 3‐mercaptopyruvate sulfurtransferase (3‐MST), key enzyme involved MSS biosynthesis. Using cells expressing mitochondrion‐localized biosensor, demonstrate this tool's ability to selectively enhance MSS. While H S was previously known suppress human immunodeficiency virus (HIV‐1), found that profoundly affected HIV‐1 life cycle, mediating viral reactivation latency. Additionally, provide evidence role host's state, membrane potential, apoptosis, respiration rates managing latency reactivation. Together, dynamic fluctuations pool have possibly conflicting effect on precision tools developed herein allow orthogonal generation within both mitochondria cytosol will be useful interrogating disease biology.

Language: Английский

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PEG-SeNPs as therapeutic agents inhibiting apoptosis and inflammation of cells infected with H1N1 influenza A virus

Scientific Reports, Journal Year: 2024, Volume and Issue: 14(1)

Published: Sept. 12, 2024

The rapid variation of influenza challenges vaccines and treatments, which makes an urgent task to develop the high-efficiency low-toxicity new anti-influenza virus drugs. Selenium is one essential trace elements for human body that possesses a good antiviral activity. In this study, we assessed A (H1N1) activity polyethylene glycol (PEG)-modified gray selenium nanoparticles (PEG-SeNPs) on Madin-Darby Canine Kidney (MDCK) cells in vitro. CCK-8 assay showed PEG-SeNPs had protective effect H1N1-infected MDCK cells. Moreover, significantly reduced mRNA level H1N1. TUNEL-DAPI test DNA damage reached high but effectively prevented after treatment. Meanwhile, JC-1, Annexin V-FITC cell cycle demonstrated apoptosis induced by H1N1 was greatly when treated with PEG-SeNPs. Furthermore, downregulation p-ATM, p-ATR P53 protein, along upregualation AKT protein indicated could inhibit H1N1-induced through reactive oxygen species (ROS)-mediated related signaling pathways. Finally, Cytokine detection inhibited production pro-inflammatory factors infection, including IL-1β, IL-5, IL-6, TNF-α. To sum up, might become potential anti-H1N1 drug due its anti-inflammatory

Language: Английский

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