In summary, our data suggested that for the treatment of genotype 1 CHC patients failed to 24-week PEG-IFN/RBV combination therapy, retreatment with a 48-week combination therapy of PEG-IFN plus RBV could be considered because a ∼50% rate of SVR is anticipated in relapsers. IL28B genotype influenced the retreatment outcomes, Napabucasin concentration particularly among those subjects not achieving RVR. Finally, for patients with unfavorable IL28B genotype and not achieving RVR or cEVR, the SVR was low and further effective treatment strategy

should be developed. Table S1 Features of 75 chronic hepatitis C (CHC) genotype 1 patients according to different interleukin-28B (IL28B) genotype. Table S2 Logistic regression analysis of factors associated with this website rapid virologic response (RVR) and sustained virologic response (SVR). Table S3 Prediction of sustained virologic response (SVR) by interleukin-28B (IL28B) genotype and/or viral kinetics. “
“We read with great interest the article by Vibert et al. 1 regarding their experience with liver transplantation (LT) for hepatocellular carcinoma

(HCC) in patients also infected with human immunodeficiency virus (HIV). It was very interesting to note that the authors reported the widest single-center experience in this field so far, focusing on an intent-to-treat analysis comparing HIV-positive and HIV-negative MycoClean Mycoplasma Removal Kit patients listed for LT. The main message from

this experience is that HIV-positive patients are characterized by a higher dropout rate while on the waiting list, thus impairing the intent-to-treat analysis without a significant impact on the overall survival and HCC recurrence in comparison with the control group. However, in considering only the HIV-positive patients who underwent transplantation, three (19%) of 16 patients were outside the Milan criteria and one (6%) of 16 patients was outside the University of California San Francisco (UCSF) criteria. Immunosuppressive therapy was based on calcineurin inhibitors (cyclosporine or tacrolimus) in all patients. It is not clear to us why these patients, with a higher tumor burden, did not receive an mTOR (mammalian target of rapamycin) inhibitor–based immunosuppressive regimen. In vitro2, 3 as well as in vivo4, 5 studies have shown the strong antitumor effect of rapamycin. In addition, as we reported in a previous article,6 rapamycin is able to inhibit HIV progression, both reducing CCR5 gene expression on the surface of both lymphocytes and macrophages and interfering with the ability of differentiating monocytes to become susceptible targets for HIV infection. Furthermore, it is well-established that the HIV TAT protein, that is secreted by HIV infected cells and taken up by normal cells, drives hepatocarcinogenesis in patients with cirrhosis.