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Tìm kiếm cho các phương pháp điều trị kháng virus mới | 73 BMS-790052, hiện đang trong giai đoạn thử nghiệm lâm sàng II kết hợp với SoC. Nó cũng được sử dụng kết hợp với một chất ức chế protease (BMS-650032) retreatment không đáp ứng trước để SoC với kết quả tốt, nhưng chỉ gắn với PegIFN / RBV. | Searching for new antiviral therapies 73 is BMS-790052 currently in phase II clinical trial in combination with SoC. It was also used in combination with a protease inhibitor BMS-650032 for retreatment of previous nonresponders to SoC with good results but only in association with PegIFN RBV. Exclusion of SoC from the therapeutic regimen resulted in high rates of viral breakthrough through week 12. Host cyclophilins inhibitors Another interesting therapeutic approach is directed at host factors important in the viral life cycle. The most promising target are cyclophilins a family of highly conserved cellular peptidyl-prolyl isomerases PPIase involved in many cellular processes such as protein folding and trafficking. Cyclophilin inhibitors block the interaction of cyclophilins with HCV proteins and hence the formation of a functional viral replication complex. Currently several non-immunosuppressive cyclosporin analogs are being tested. The most potent seems to be Alisporivir Debio-025 tested in both HCV monoinfected and HIV HCV coinfected patients with promising results. The combination of Debio 025 and PegIFN-a2a showed a significant VL reduction after 28 days in patients infected with genotypes 1 3 and 4 Flisiak 2009 . Such host protein-targeting compounds have the advantage of higher genetic barriers to resistance and could be instrumental in future IFN-free regimens Table 4.3 . Emergence of drug resistant mutations High levels of baseline drug resistance mutations in the NS3 protease or NS5B polymerase were identified in a significant number of viral isolates from treatment-naive patients. Moreover there seem to be differences between HCV genotypes subtypes in terms of the frequencies of baseline mutations and natural polymorphisms which can translate into distinct susceptibility to DAAs. An overlap of immune escape and drug resistance profiles has also been reported Gaudieri 2009 . This is trial version www.adultpdf.com 74 Hepatitis C Treatment The majority .
