approximate or exceed the total number of human cells, highlighting the profound extent of microbial colonization [1; 2; 3]. The microbiota plays a fundamental role in maintaining homeostasis by contributing to metabolic functions, synthesizing essential nutrients, and engaging in immunomodulatory activities that shape host defense mechanisms. The intestinal microbiota, in particular, is indispensable for the proper development of the immune system, influencing immune tolerance and enhancing the host's ability to recognize and eliminate pathogenic invaders. The relationship between host immunity and gut microbiota is increasingly recognized as a critical determinant of health and disease, with growing evidence implicating microbial dysbiosis--an imbalance in microbial composition--in the progression of various chronic conditions, including hepatic disorders [4; 5]. One area of emerging scientific interest is the potential involvement of intestinal microbiota in the pathogenesis of chronic liver diseases associated with hepatitis C virus (HCV) infection. HCV remains a major global health burden, often leading to progressive hepatic fibrosis, cirrhosis, and hepatocellular carcinoma. Despite advances in antiviral therapies, the underlying mechanisms through which the gut microbiota influences the persistence and progression of chronic HCV infection remain incompletely understood, warranting further investigation [6]. The dynamic interplay between microbiota and viral pathogens extends beyond simple coexistence; microbiota can actively modulate viral pathogenesis through multiple mechanisms, including direct interactions with viral particles, competition for nutrients and ecological niches, and the regulation of host immune responses. The influence of microbiota on viral infections is multifaceted and remains a subject of ongoing debate. Certain microbial species may exert antiviral effects by producing metabolites that inhibit viral replication or enhance antiviral immune responses. Conversely, other microbial components may facilitate viral persistence by suppressing immune activation or by modulating the integrity of epithelial barriers, thereby influencing viral dissemination within the host. It is also conceivable that microbiota may exert a neutral effect, neither enhancing nor inhibiting viral infections, depending on the specific host and environmental context [7; 8; 9; 10]. In the case of HCV infection, microbiota-derived metabolites and bacterial components, such as lipopolysaccharidesaccharides, have been implicated in shaping hepatic immune responses and inflammatory pathways. Additionally, the gut-liver axis--a bidirectional communication network between the intestinal microbiota and the liver--plays a central role in liver disease progression. Disruptions in this axis, particularly in the context of gut dysbiosis and increased intestinal permeability, have been associated with heightened systemic inflammation and hepatic fibrosis, further underscoring the relevance of microbiota in chronic HCV pathogenesis [11; 12; 13; 14]. Beyond viral infections, intestinal microbiota has been widely acknowledged as a key player in the development and progression of autoimmune diseases, including type 1 diabetes (T1D), wherein microbial alterations contribute to immune dysregulation and the breakdown of self-tolerance [15; 16; 17]. Given the parallels between immune dysfunction in autoimmune disorders and chronic viral infections, it is plausible that microbiota-mediated immune modulation similarly influences the trajectory of HCV-related liver diseases. The objective of this review is to synthesize current knowledge regarding microbiota-HCV interactions and to critically assess the potential mechanistic pathways through which microbiota may influence HCV infection and its associated pathologies.