High throughput sequencing techniques could be used to obtain sufficient sequence coverage, but the lengths of reads might be too short to allow de novo assembly, and the method

of mapping to the reference HCV genome could be detecting the full-length HCV sequence. NGS technology Cisplatin mouse is a powerful tool for obtaining more profound insight into the dynamics of genetic variants in the HCV quasispecies in human serum.[26] Currently, potential treatments in development include drugs that target the HCV NS3/4A serine protease and the NS5B RNA-dependent RNA polymerase referred to as direct-acting antiviral agent (DAA).[27] These drugs have been evaluated in clinical trials alone and in combination with pegylated interferon and ribavirin.[28] Therefore, detecting the frequency of drug-resistant HCV variants prior to treatment is important. In treatment-naïve patients, the frequency of all

resistant variants of NS3 was generally found to be below 1% using the 454 GS series[29, 30] or by the Illumina Genome sequencer.[31] Viral dynamics have emerged whereby drug-resistant variants frequently appear, but are rapidly lost in the absence of selective this website pressure because of reduced fitness. Results using NGS technology have also suggested that not only the number but also the nature of the nucleotide changes can contribute to the genetic barriers to the development of resistance to DAAs.[32] Using

a genetically engineered HCV infection system in a chimeric mouse model, the rapid emergence of DAA-resistant HCV variants was induced by mutation from a wild-type strain of HCV in vivo.[33] Other 454 GS series sequencer studies showed that analysis of the PKR-elf2α phosphorylation homology domain MCE公司 sequence before or during treatment cannot be used to reliably predict the outcome of treatment in patients co-infected with HCV genotype 1 and HIV,[34] and highlighted the genetic diversity of HCV, which enables it to evade the host immune system.[35] Concerning the within-host evolution of HCV during infection, the genetic diversity of viral variants showed strong selective forces that limit viral evolution in the acute phase of infection.[36, 37] Taking nucleoside/nucleotide analogs (NA) is a major antiviral therapy for the treatment of chronic HBV infection.[38] They inhibit the viral polymerase activity by interfering with the priming of reverse transcription and elongation of the viral minus or plus strand DNA.[39] The problem is that these treatments are hampered by the selection of drug-resistant mutants, leading to a loss of efficacy, viral relapse and exacerbations of hepatitis after discontinuation.[40] Using NGS, drug-resistant mutations of HBV minor variants can be identified.