Viral Infections as Triggers of Organ Fibrosis and Chronic Tissue Remodeling: Immune-Mediated Mechanisms linking Inflammation, Fibrogenesis, and Long-Term Organ Dysfunction

Viral immunopathology and fibrogenesis research has revealed that viral infections can instigate long-lasting structural and functional alterations across multiple organs. Traditionally, fibrosis was examined chiefly in chronic liver diseases associated with hepatitis viruses, but recent advances broaden its relevance to diverse tissues, including the lung, heart, kidney, brain, bone marrow, and vascular networks. Current evidence demonstrates that persistent immune activation, through chronic inflammation, mitochondrial impairment, and cellular senescence, leads to maladaptive repair, stromal dysfunction, extracellular matrix remodeling, and fibrosis. Despite accumulating clinical data, the precise immune-mediated mechanisms driving these processes and their contribution to organ-specific outcomes remain incompletely understood. Emerging multi-omics studies and post-viral clinical syndromes, such as those following SARS-CoV-2 infection, have underscored the pressing need for an integrative view bridging immunology, virology, and regenerative biology.This Research Topic aims to elucidate the cellular and molecular mechanisms linking viral infection, immune dysregulation, and the cascade of fibrotic remodeling that culminates in long-term organ dysfunction. By bringing together multidisciplinary expertise from immunology, pathology, virology, and systems biology, it seeks to clarify how viral persistence and host responses co-evolve to produce chronic tissue injury. Key goals include identifying molecular checkpoints that connect immune activation to fibroblast reprogramming, defining biomarkers of post-viral fibrogenesis, and exploring translational routes to prevent or reverse organ fibrosis. Questions surrounding macrophage polarization, T-cell exhaustion, inflammasome activity, and the contribution of senescence and ferroptosis to fibrogenic signalling will be central to this investigation.To gather further insights into virus-induced fibrotic and remodeling processes across organs while maintaining mechanistic focus, we welcome contributions spanning basic, translational, and clinical science. Submissions are encouraged that dissect molecular and cellular interactions, organ-specific phenotypes, and cross-cutting immunometabolic pathways involved in long-term post-viral outcomes. We welcome articles addressing, but not limited to, the following themes:o Mechanisms of organ-specific fibrogenesis triggered by viral infectiono Immune-mediated pathways driving chronic inflammation and tissue remodelingo Macrophage polarization, senescence, and immune-stromal cross-talk in fibrogenesiso Persistent viral reservoirs, inflammaging, and chronic inflammatory microenvironmentso Fibrotic and degenerative remodeling of liver, lung, heart, kidney, CNS, and vascular tissueso Extracellular vesicle signaling and intercellular communication in viral tissue injuryo Mitochondrial dysfunction, ferroptosis, oxidative stress, and metabolic reprogrammingo Post-viral syndromes, including Long COVID and persistent organ dysfunctiono Imaging and biomarker approaches for fibrotic progression and tissue repairo Therapeutic and regenerative interventions targeting fibrosis or immune dysregulation Topic editors: Jorge Quarleri, M. Victoria Delpino, Enrique Roberto Argañaraz Source: https://www.frontiersin.org/research-topics/82242/viral-infections-as-triggers-of-organ-fibrosis-and-chronic-tissue-remodeling-immune-mediated-mechanisms-linking-inflammation-fibrogenesis-and-long-term-organ-dysfunction