Bystander Effects and Profibrotic Interactions in Hepatic Stellate Cells during HIV and HCV Coinfection DOI Creative Commons
Cintia Cevallos,

Patricio Jarmoluk,

Franco Agustín Sviercz

et al.

Journal of Immunology Research, Journal Year: 2024, Volume and Issue: 2024, P. 1 - 14

Published: April 30, 2024

This study aims to explore the influence of coinfection with HCV and HIV on hepatic fibrosis. A coculture system was set up actively replicate both viruses, incorporating CD4 T lymphocytes (Jurkat), stellate cells (LX-2), hepatocytes (Huh7.5). LX-2 cells’ susceptibility infection assessed through measurements receptor expression, exposure cell-free virus, cell-to-cell contact HIV-infected Jurkat cells. The evaluated profibrotic parameters, including programed cell death, ROS imbalance, cytokines (IL-6, TGF-β, TNF-α), extracellular matrix components (collagen, α-SMA, MMP-9). impact LX-2/HIV-Jurkat examined using soluble factors released from HCV-infected hepatocytes. Despite being nonsusceptible direct infection, bystander effects were observed, leading increased oxidative stress dysregulated cytokine release. Coculture intensified fibrosis, redox expression cytokines, production. Conversely, Huh7.5 exhibited elevated gene transcriptions but without measurable coculture. highlights how worsen fibrosis during HCV/HIV coinfection. They increase stress, levels, production in factors. These insights offer valuable potential therapies for coinfected individuals.

Language: Английский

Bystander Effects and Profibrotic Interactions in Hepatic Stellate Cells during HIV and HCV Coinfection DOI Creative Commons
Cintia Cevallos,

Patricio Jarmoluk,

Franco Agustín Sviercz

et al.

Journal of Immunology Research, Journal Year: 2024, Volume and Issue: 2024, P. 1 - 14

Published: April 30, 2024

This study aims to explore the influence of coinfection with HCV and HIV on hepatic fibrosis. A coculture system was set up actively replicate both viruses, incorporating CD4 T lymphocytes (Jurkat), stellate cells (LX-2), hepatocytes (Huh7.5). LX-2 cells’ susceptibility infection assessed through measurements receptor expression, exposure cell-free virus, cell-to-cell contact HIV-infected Jurkat cells. The evaluated profibrotic parameters, including programed cell death, ROS imbalance, cytokines (IL-6, TGF-β, TNF-α), extracellular matrix components (collagen, α-SMA, MMP-9). impact LX-2/HIV-Jurkat examined using soluble factors released from HCV-infected hepatocytes. Despite being nonsusceptible direct infection, bystander effects were observed, leading increased oxidative stress dysregulated cytokine release. Coculture intensified fibrosis, redox expression cytokines, production. Conversely, Huh7.5 exhibited elevated gene transcriptions but without measurable coculture. highlights how worsen fibrosis during HCV/HIV coinfection. They increase stress, levels, production in factors. These insights offer valuable potential therapies for coinfected individuals.

Language: Английский

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