Norovirus-mediated translation repression promotes macrophage cell death DOI Creative Commons
Turgut E. Aktepe,

Joshua M. Deerain,

Jennifer Hyde

et al.

PLoS Pathogens, Journal Year: 2024, Volume and Issue: 20(9), P. e1012480 - e1012480

Published: Sept. 3, 2024

Norovirus infection is characterised by a rapid onset of disease and the development debilitating symptoms including projectile vomiting diffuse diarrhoea. Vaccines antivirals are sorely lacking developments in these areas hampered lack an adequate cell culture system to investigate human norovirus replication pathogenesis. Herein, we describe how model norovirus, Mouse (MNV), produces viral protein, NS3, with functional capacity attenuate host protein translation which invokes activation death via apoptosis. We show that this function NS3 conserved between mouse viruses map domain attributable function. Our study highlights critical mediates crucial activities during replication, potentially identifying as worthy target for antiviral drug development.

Language: Английский

Targeting MCL1 with Sanggenon C overcomes MCL1-driven adaptive chemoresistance via dysregulation of autophagy and endoplasmic reticulum stress in cervical cancer DOI
Wei Sun,

Huarui Cai,

Kui Zhang

et al.

Phytomedicine, Journal Year: 2024, Volume and Issue: 133, P. 155935 - 155935

Published: Aug. 3, 2024

Language: Английский

Citations

4
Dendritic cells activate pyroptosis and effector-triggered apoptosis to restrictLegionellainfection DOI Open Access
Víctor R. Vázquez Marrero, Jessica Doerner, Kimberly A. Wodzanowski

et al.

bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 17, 2025

Abstract The innate immune system relies on pattern recognition receptors (PRRs) to detect pathogen-associated molecular patterns (PAMPs) and guard proteins monitor pathogen disruption of host cell processes. How different types engage PRR- protein-dependent defenses in response infection is poorly understood. Here, we show that macrophages dendritic cells (DCs) respond distinct ways bacterial virulence activities. In macrophages, the Legionella pneumophila deploys its Dot/Icm type IV secretion (T4SS) deliver effector facilitate robust intracellular replication. contrast, T4SS activity triggers rapid DC death potently restricts replication within this type. Intriguingly, found infected DCs exhibit considerable heterogeneity at single level. Initially, a subset activate caspase-11 NLRP3 inflammasome-dependent pyroptosis release IL-1 β early during infection. At later timepoints, separate population undergoes apoptosis driven by effectors block protein synthesis, thereby depleting levels pro-survival Mcl-1 cFLIP. Together, effector-triggered robustly restrict DCs. Collectively, our work suggests model where cFLIP translation DCs, distinctly employ sensors mount divergent responses

Language: Английский

Citations

0
Comparative transcriptome analysis reveals distinct immune response in different ploidy cyprinid caudal fin cells following SVCV infection DOI
Dan Zeng, Kai Yao, Yixin Chen

et al.

Aquaculture, Journal Year: 2025, Volume and Issue: unknown, P. 742365 - 742365

Published: March 1, 2025

Language: Английский

Citations

0
Bid Protein: A Participant in the Apoptotic Network with Roles in Viral Infections DOI Open Access
Zbigniew Wyżewski, Karolina P. Gregorczyk-Zboroch, Matylda Barbara Mielcarska

et al.

International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(6), P. 2385 - 2385

Published: March 7, 2025

The BH3-interacting domain death agonist (Bid), a proapoptotic signaling molecule of the B-cell lymphoma 2 (Bcl-2) family, is key regulator mitochondrial outer membrane (MOM) permeability. Uniquely positioned at intersection extrinsic and intrinsic apoptosis pathways, Bid links receptor to mitochondria-dependent cascade can also be activated by endoplasmic reticulum (ER) stress. In its active forms, cleaved (cBid) truncated (tBid), it disrupts MOM integrity via Bax/Bak-dependent independent mechanisms. Apoptosis plays dual role in viral infections, either promoting or counteracting propagation. Consequently, viruses modulate favor their replication. deregulation activity contributes oncogenic transformation, inflammation, immunosuppression, neurotoxicity, pathogen propagation during various infections. this work, we explore Bid’s structure, function, activation processes, targeting. We describe induction involvement infections with multiple viruses. Additionally, discuss therapeutic potential antiviral strategies. Understanding pathways offers valuable insights into host–virus interactions pathogenesis This knowledge may facilitate development novel approaches combat virus-associated diseases effectively.

Language: Английский

Citations

0
Norovirus-mediated translation repression promotes macrophage cell death DOI Creative Commons
Turgut E. Aktepe,

Joshua M. Deerain,

Jennifer Hyde

et al.

PLoS Pathogens, Journal Year: 2024, Volume and Issue: 20(9), P. e1012480 - e1012480

Published: Sept. 3, 2024

Norovirus infection is characterised by a rapid onset of disease and the development debilitating symptoms including projectile vomiting diffuse diarrhoea. Vaccines antivirals are sorely lacking developments in these areas hampered lack an adequate cell culture system to investigate human norovirus replication pathogenesis. Herein, we describe how model norovirus, Mouse (MNV), produces viral protein, NS3, with functional capacity attenuate host protein translation which invokes activation death via apoptosis. We show that this function NS3 conserved between mouse viruses map domain attributable function. Our study highlights critical mediates crucial activities during replication, potentially identifying as worthy target for antiviral drug development.

Language: Английский

Citations

1