## 9 Conclusions  
Research exploring the complex interactions between human microbiota and hepatitis C virus (HCV) infections remains relatively limited. However, the existing body of literature offers valuable insights that could inform future investigations and contribute to the development of theoretical frameworks in this field. HCV infection, along with its progression to chronic liver diseases such as fibrosis, cirrhosis, and HCC, has been increasingly linked to alterations in gut microbiota composition. These alterations are often characterized by dysbiosis, a condition marked by disruptions in microbial diversity and imbalances in bacterial phyla. A growing body of evidence suggests that gut microbial dysbiosis plays a critical role in the pathogenesis of HCV-related liver complications. The gut-liver axis--a bidirectional communication system between the gastrointestinal tract and the liver--facilitates the exchange of microbial metabolites, endotoxins, and inflammatory mediators. This axis is particularly relevant in HCV infection, as bacterial translocation and the leakage of microbial products from the intestine into the portal circulation have been implicated in exacerbating liver inflammation, promoting fibrosis, and contributing to the progression of liver disease. Notably, studies have identified reductions in beneficial bacterial taxa, such as those within the Firmicutes and Bacteroidetes phyla, alongside an increase in potentially pathogenic bacteria, including members of the Proteobacteria phylum, in patients with chronic HCV infection. These compositional shifts may influence systemic immune responses, modulate hepatic inflammation, and disrupt metabolic homeostasis, further complicating the course of HCV-related diseases. Given the established role of the gut microbiota in maintaining immune homeostasis and liver function, therapeutic strategies aimed at restoring microbial equilibrium have garnered significant interest. One such intervention is fecal microbiota transplantation (FMT), which involves the transfer of a healthy donor's gut microbiota to a recipient exhibiting dysbiosis. FMT has demonstrated efficacy in modulating gut microbial diversity, reducing inflammation, and improving metabolic parameters in various liver diseases, including non-alcoholic fatty liver disease (NAFLD) and cirrhosis. Therefore, it may hold therapeutic potential for HCV-infected patients experiencing gut dysbiosis, particularly those with advanced liver disease. However, while FMT represents a promising approach, its application in the context of HCV remains largely unexplored. Further research is required to determine its efficacy, optimal protocols, and long-term outcomes in this patient population. A fundamental question that remains unresolved is whether dysbiosis precedes and exacerbates HCV infection or if chronic HCV infection itself drives microbial alterations. It is possible that pre-existing gut microbial imbalances create a microenvironment conducive to viral persistence and immune dysregulation, thereby predisposing individuals to more severe HCV-related liver damage. Conversely, chronic HCV infection, through mechanisms such as immune-mediated inflammation, hepatic metabolic alterations, and bile acid dysregulation, may contribute to progressive changes in gut microbiota composition. Longitudinal studies and mechanistic investigations are essential to elucidate the causal relationships between HCV infection and microbiota alterations, which could pave the way for microbiome-targeted interventions in the management of HCV-associated liver diseases. In summary, while the current understanding of microbiota-HCV interactions is limited, emerging evidence underscores the critical role of the gut-liver axis in shaping the course of HCV infection and its complications. The potential therapeutic benefits of microbiome-modulating strategies, including FMT, warrant further exploration in the context of HCV.