Hepatitis C virus (HCV) infection is a global health concern, chronically affecting over 71 million people. It primarily targets the liver but also causes systemic complications through inflammation, oxidative stress, and metabolic dysregulation. HCV is a highly variable RNA virus with six major genotypes that are mainly transmitted via blood. Often asymptomatic, the infection progresses silently to chronic hepatitis C (CHC), which can lead to fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). Direct-acting antivirals (DAAs) have revolutionized treatment, achieving cure rates above 95%, improving liver function, reversing fibrosis, and normalizing metabolism. HCV disrupts iron metabolism by suppressing hepcidin, causing iron overload and oxidative stress. It also alters lipid metabolism, inducing steatosis, and affects glucose metabolism, contributing to insulin resistance and type 2 diabetes. DAAs improve these metabolic outcomes. HCV promotes oxidative stress via viral proteins, damaging liver cells and DNA and triggering inflammation and fibrogenesis. Even post-cure, oxidative stress and iron overload may continue to drive disease progression. Genetic and epigenetic factors influence fibrosis progression and HCC risk. Despite a sustained virologic response (SVR), patients with advanced liver damage remain at risk for HCC and metabolic diseases, highlighting the need for continued monitoring and personalized post-treatment care.

Heart failure (HF) is frequently associated with iron deficiency and anemia, negatively impacting patient outcomes. This study aimed to investigate the contribution of genetic variation in iron metabolism-related genes to biochemical and hematological phenotypes in HF. An HF population of 182 patients with functional iron deficiency (ID) and anemia was stratified by sex and heart failure subtype, including HF with reduced ejection fraction (HFrEF) and HF with non-reduced ejection fraction (HFnrEF). Genetic variants in HFE (rs1799945), SLC40A1 (rs1439816, rs2304704), and TMPRSS6 (rs855791) were evaluated. Variants in HFE and SLC40A1 were associated with differences in serum iron, ferritin, transferrin saturation, hemoglobin, and RDW. The phenotypic impact of these variants was modulated by sex and heart failure subtype, highlighting the influence of iron availability, inflammatory burden, and erythropoietic demand. In contrast, no significant associations were observed for the TMPRSS6 variant. In conclusion, genetic variation in key regulators of iron metabolism contributes to the heterogeneity of iron-related biochemical and hematological phenotypes in HF. These findings emphasize the interplay between genetic background, sex, and heart failure physiology and support the relevance of personalized approaches to iron assessment and management in heart failure.

Human papillomavirus (HPV) infection plays a crucial role in cervical carcinogenesis. The link between the autonomic nervous system and tumor biology is increasingly being recognized. Understanding how neural signaling pathways interact with HPV oncogenesis could open new avenues for therapeutic intervention. We aim to study the contribution of the autonomic nervous system-related genes to the HPV-associated cervical lesions. A population of 140 HPV-infected women presenting cervical lesions was compared to a control population. Genes/variants under study were: BDNF/rs6265, NTRK2/rs2289656, NGF/rs6330, SLC6A4/5-HTT variable number tandem repeats intron 2, HTR2A/rs6313, ADRBR2/rs1042713, and CHRNA5/rs16969968. Samples were genotyped using polymerase chain reaction (PCR), PCR-restriction fragment length polymorphism, and endpoint genotyping. Statistical analysis revealed a genetic contribution for SCL6A4, ADRB2, and CHRNA5. SCL6A4 showed statistically significant association in the codominant (p=0.003) and dominant models (p=0.024, odds ratio [OR] = 2.301). ADRB2 showed statistically significant association in the codominant (p<0.001), dominant (p=0.024, OR = 4.728), recessive (p<0.001, OR = 4.856), and allelic models (p<0.001, OR = 4.091), while CHRNA5 showed statistically significant association in the dominant model (p=0.030, OR = 0.529). We conclude that there is a genetic contribution of the adrenergic (ADRB2), cholinergic (CHRNA5), and serotonergic (SLC6A4) systems to cervical lesions associated with HPV infections.