Abstract
essentially hepatotropic, recent studies suggest that it can also infect peripheral blood mononuclear cells (PBMC). HCV infection has been clinically associated with serum lipid abnormalities. The aim of this study is to analyze the possible roles of genes involved in HCV-mediated lipid metabolism in PBMC from HCV infected patients. Materials and Methods: Using The Human Adipogenesis RT ProfilerTM PCR Array, we have analyzed the expression profile of 84 genes in chronic HCV PBMCs patients normalized with PBMCs from heathy donors. To compared the results obtained from HCV+ PBMCs with the expression in the hepatocytes, we have used a JFH1/HCV in vitro system after 48h post infection normalized with uninfected Huh 7.5.1 cell line. Results: Both in vivo and in vitro models HCV was able to upregulate the same genes (14% in both of them) involved in lipid metabolism such as SREBP1c, FASN, FABP4, ACACB and in signal transduction (29% and 27% respectively) resulted modulated both in HCV PBMCs and J6/JFH1-infection system. In both models the Kruppel-like transcription factor 15 (KLF15). KLF15 results significantly upregulated in HCV+ PBMCs as well as the J6/JFH1 in vitro infection. In addition, in PBMCs, KLF15 upregulation is statistically and positively correlated to the Body Weight, the BMI and the ALT levels. Furthermore, in PBMCs from HCV+ donors, KLF15 expression correlates with the HCV Viral Load and the antibody titer (anti-NS3 anti-NS4 and anti-capsid), suggesting a possible intriguing role of this factor in HCV infection. Conclusions: Our results confirm the ability of HCV to affect lipid metabolism; we have highlighted a similar modulation both in HCV patients lymphoid cells and in J6/JFH1 HCV infection model. In particular, the virus-related KLF15 enhanced expression, in both in vivo and in vitro models, suggests this protein as new possible marker of HCV infection and as a potential therapeutic target useful to counteract HCV infection.
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