Predictors of Sustained Virological Response (SVR) in Patients with Advanced Chronic Hepatitis C (CHC) Treated with Current Direct Acting Antiviral(s) (DAA). Heraclis: Hellenic Multicenter Real-Life Cohort Study

Papatheodoridis, George V.; Manolakopoulos, Spilios; Kapatais, Andreas; Sinakos, Emanuel; Elefsiniotis, Ioannis; Goulis, John; Deutsch, Melanie; Vlachogiannakos, John; Dalekos, George Ν.; Koskinas, John; Karatapanis, Stylianos; Schina, Maria; Manesis, Emanuel K.; Ketikoglou, I.; Sevastianos, V.; Triantos, Christos; Papageorgiou, Maria-Vasiliki; Κourikou, Αnastasia; Karaoulani, T.; Evangelidou, Eftychia; Koukoufiki, Argyro; Karagiannakis, Dimitrios; Gatselis, Nikolaos; Tampaki, Maria; Ntetskas, Georgios; Tsolias, Chrisostomos; Voulgaris, Theodoros; Ioannidou, Panagiota; Akriviadis, Evangelos

doi:10.1016/s0016-5085(17)33683-1

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“…Viral factors that were associated with worse response included non-genotype-2 infection, high viral load, and unfavourable viral kinetics during treatment. 4,20 Some authors have revealed that hepatitis viruses infection might play a role in fast-tracking the methylation process which is involved in HCC development, and affect its response to treatment. 6,19,21,22 Progression from chronic hepatic inflammation to the fibrotic/cirrhotic stage is supported by numerous core pathways, observed in other fibrotic diseases, as well as tissue-or injuryspecific pathways that are only activated in particular conditions.…”

Section: Discussionmentioning

confidence: 99%

Influence of some methylated hepatocarcinogenesis-related genes on the response to antiviral therapy and development of fibrosis in chronic hepatitis C patients

et al. 2020

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Background/Aims: Epigenetics involved in multiple normal cellular processes. Previous research have revealed the role of hepatitis C virus infection in accelerating methylation process and affecting response to treatment in chronic hepatitis patients. This work aimed to elucidate the role of promoter methylation (PM) in response to antiviral therapy, and its contribution to the development of fibrosis through hepatocarcinogenesis-related genes. Methods: A total of 159 chronic hepatitis Egyptian patients versus 100 healthy control group were included. The methylation profile of a panel 9 genes (SFRP1, p14, p73, APC, DAPK, RASSF1A, LINE1, O6MGMT, and p16) was detected in patients' plasma using methylation-specific polymerase chain reaction (MSP). Results: Clinical and laboratory findings were gathered for patients with combined pegylated interferon and ribavirin antiviral therapy. Regarding the patients' response to antiviral therapy, the percentage of non-responders for APC, O6MGMT, RASSF1A, SFRP1, and p16 methylated genes were significantly higher versus responders (P<0.05). Of the 159 included patients, the most frequent methylated genes were SFRP1 (102/159), followed by p16 (100/159), RASSF1A (98/159), then LINE1 (81/159), P73 (81/159), APC (78/159), DAPK (66/159), O6MGMT (66/159), and p14 (54/159). A total of 67/98 (68.4%) cases of RASSF1A methylated gene (P=0.0.024), and 62/100 (62%) cases of P16 methylated gene (P=0.03) were associated with mild-degree fibrosis. Conclusions: To recapitulate, the PM of SFRP1, APC, RASSF1A, O6MGMT, and p16 genes increases in chronic hepatitis C patients, and can affect patients' response to antiviral therapy. The RASSF1A and P16 genes might have a role in the distinction between mild and marked fibrosis.

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