## 6 Microbiota Alterations in HCV Patients
Furthermore, it is well established that chronic HCV patients experience an increase in the phylum Bacteroidetes, the family Enterobacteriaceaeae, and viridans streptococci, alongside a decrease in the phylum Firmicutes. It is also important to note that HCV infection is linked to elevated serum levels of lipopolysaccharidesacharides (LPSs), which suggest a compromised intestinal barrier, microbial translocation, and inflammation as the disease progresses [42]. Interestingly, since the intestinal microbiota was shown to be a powerful tool in balancing the immune system homeostasis, it is reasonable to consider it as a promising means to help the body counteract viral infections, such as HCV. Considering this, probiotic administration to HCV patients could enhance antiviral therapy efficacy by sustaining the immune system [45]. On the other hand, dysbiosis impacts the integrity of the gut barrier, resulting in increased bacterial translocation. This process can lead to infections, systemic inflammation, and vasodilation, all of which play a significant role in acute decompensation and subsequent fibrosis, cirrhosis, and organ failure [46]. Furthermore, the onset and advancement of viral hepatitis are associated with a notable reduction in the diversity of gut microbiota. This decline in gut microbial alpha diversity, along with an elevated presence of genera such as Butyricimonas, Escherichia Shigella, Veillonella, and Lactobacillus, holds significant promise as a potential biomarker for assessing the risk of viral hepatitis [47]. Such findings could be the foundation for elaborating a well-founded microbiota-based predictive HCV diagnostic system. Since the diversity and composition of gut microbiota are significantly influenced by both macronutrients, including fiber, protein, and fatty acids, and micronutrients, such as vitamins and minerals [48], and knowing Butyricimonas, Escherichia-Shigella, Veillonella, and Lactobacillus are potential HCV biomarkers, it could be reasonable to think of diet as an HCV infection risk factor. From a risk point of view, commensal bacteria, primarily anaerobic in nature, play a crucial role in preserving microbial equilibrium and resistance to colonization by inhibiting the proliferation of pathogenic bacteria. This is achieved through complex interactions within the microbial community and between the microbiota and the host. In individuals experiencing immune suppression as a result of high-dose chemotherapy or hematopoietic stem cell transplantation, the use of antibiotics can disrupt the microbiota. This disruption, combined with compromised host immunity, creates conditions that favor the dominance of pathogenic species in the intestines, resulting in heightened bacterial translocation and an increased risk of systemic infections. After these considerations, it is safe to infer that microbiota-targeted interventions could be harmful in immunocompromised HCV patients [49]. Since variations in gut microbiota attributable to geographic location and seasonal fluctuations are closely associated with alterations in dietary patterns, and knowing that even minor adjustments to one's diet can have a profound effect on the composition of the gut microbiota, we could consider such parameters as related to microbiota-HCV interactions [50]. To further elucidate the evolving landscape of research on gut microbiota alterations in HCV-infected patients, Table 1 provides an overview of the most up-to-date clinical trials investigating the relationship between HCV infection and gut microbiota dysbiosis. These studies aim to enhance our understanding of microbiota-mediated mechanisms in HCV pathogenesis and explore novel microbiota-based therapeutic interventions.