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The new antivirals for the treatment of hepatitis C virus (HCV) are characterised by short duration with an increased sustained virological response (SVR), a reduced follow-up with a significant impact on HCV natural history and health public burden. However they still lack substantial data on long-term disease evolution in real life.1 More recently Yin et al showed that real-life SVR was similar to clinical study with a reduction in health costs.2 However, despite the noteworthy results on the virus, the long-term outcome, possible related adverse drug reaction (ADR) and their impact on healthcare cost are still controversial, even when achieving SVR3 particularly in regards to hepatocellular carcinoma (HCC). At the beginning of 2015, we started to assess the presence of any kind of ADR of these new DAAs …

Background and Aim: Hepatitis A virus (HAV) causes a transient illness leaving permanent protection against reinfection. Few data are available on the regulatory mechanisms involved in the CD4+ T helper activation. We aimed to investigate the frequency and function of CD3+/CD4+/CD25+ T cells with regulatory function (Tregs) during acute HAV infection. Methods: We enrolled 35 consecutive patients and 15 healthy donors, enumerated Tregs by flow cytometry assay and evaluated, after immunomagnetical sorting with magnetic beads, their ability to inhibit the proliferation of CD4+/CD25– T lymphocytes at different ratios (1:1, 1:10, 1:20). Results: All patients had the usual course of infection. Our immunological analysis showed Tregs frequency in these patients (6.5% [range, 5–8.8%]; 36 [range, 10–87] cells) did not have any statistical difference compared with healthy donors (6% [range, 5–8%]; 48 (range, 23–71) cells), while their ability to suppress CD4+/CD25– was drastically reduced at different ratios (Mann–Whitney U-test; ratio 1:1, 93% vs 72%, z = −3.34, P

We conducted a long-term prospective study of 89 cancer survivor children who had acquired hepatitis B virus (HBV) and/or hepatitis C virus (HCV) during treatment for neoplasia, the aim being to evaluate the natural history of the diseases and the effect of interferon (IFN) treatment. Patients were followed up for a median period of 13 years (range, 8 to 20); 46 were infected by HBV, 11 by HCV, and 32 coinfected by HBV and HCV. A spontaneous clearance of hepatitis B surface antigen (HBsAg) occurred more frequently in coinfected patients (19%) than in the HBV-infected (2%; P = .004), with an annual seroconversion rate of 2.1% and 0.2%, respectively (P= .008). Loss of hepatitis Be antigen (HBeAg) occurred in 44% of coinfected and in 28% of HBV-infected patients. Clearance of serum HCV-RNA was observed in 34% and 9%, respectively, of coinfected and HCV-infected patients. Seventeen HBV-infected, 4 HCV-infected, and 16 coinfected patients received -IFN treatment. In the HBV group, 6 patients (35%) cleared serum HBV DNA and seroconverted to anti-HBe; in the HCV-group, none cleared HCV-RNA. In the coinfected group, 1 patient cleared both HBV DNA and HCV-RNA, 6 patients cleared serum HCV-RNA alone, and 1 only HBV DNA and HBeAg. Overall, the diseases showed a mild histological course with no evidence of liver cirrhosis. A reciprocal interference on viral replication between HBV and HCV may occur in coinfected patients. Treatment seems to be effective for selected cases and is justified in view of the uncertain prognosis of the disease in these patients.