They can only detect previously identified mutations, and these methods would need adaptation to detect mutants that confer resistance to a growing list of nucleos(t)ide reverse transcriptase inhibitors [110]. 4.2.2.4 HBV genotyping. Currently, there is no indication for performing this as standard of care, except possibly in patients being considered for interferon therapy. It may be more relevant in the future as information on the differences among genotypes emerges. HBV genotypes have been reported to

correlate with Bortezomib spontaneous and interferon-induced HBeAg seroconversion, activity of liver disease, and progression to cirrhosis and HCC [101,111,112]. For example, HBV genotypes C and D are more difficult to treat than genotypes A and B [113,114]. There is also some evidence suggesting an increased pathogenicity of genotype C over B, with a greater likelihood of developing HCC [115,116]. Much of the current data examining the clinical relevance of HBV genotype should be viewed with caution. Many studies were small and cross-sectional in design, comparing two of the major genotypes with each other, and may be affected by referral bias. The predictive values of genotype in prognosis and treatment response have not been evaluated in prospective Luminespib mw trials, and, currently, most clinicians do not base their management

decisions selleck kinase inhibitor on the viral genotype. However, this approach is likely to change as more data become available. Further studies are still needed in this area [117]. HBV is directly carcinogenic and may promote the development of HCC in the absence of cirrhosis, especially in populations where HBV may

have been acquired at birth or in early childhood [53]. High HBV viral loads and low CD4 cell counts may be linked to the development of HCC [54,55]. Screening programmes utilizing serum AFP measurements together with 6-monthly USSs have been demonstrated to improve survival in non-HIV-infected patients [57]. Treatment decisions should be guided by the algorithms in Figures 1 and 2. Central to optimal management is the need for adequate initial assessment of both HBV and HIV status to inform the decision as to whether neither, HBV alone or both viruses require treatment [118]. This includes consideration of the severity of liver disease [119]. In HBV monoinfection, the decision on who to treat is based primarily on the ALT level, liver histology, HBeAg status and HBV DNA level [118–123]. ALT normality should not be used to assume that treatment is not necessary, although raised ALT often reflects HBV-induced inflammation and the need for treatment. As significant liver damage may be present without raised liver enzymes, assessment of liver fibrosis by transient elastometry (e.g.