These include disruption of cell signaling pathways, DNA repair m

These include disruption of cell signaling pathways, DNA repair mechanisms, and apoptotic pathways.21 The key question that merits further research is whether the presence of small amounts click here of HBV truly plays an important role during hepatic carcinogenesis, or whether the above association was just a reflection of severity of liver disease. Table 1 summarizes the impact

of occult HBV infection on treatment response in CHC patients receiving antiviral therapy. Some studies have shown that occult HBV infection may provoke a reduction in the response rate to interferon (IFN) therapy in patients with CHC.11,12 However, other authors have not found any impact of occult HBV infection on the success of the therapy.8,13–16,22 The above phenomenon probably attributed to the small sample size, heterogeneity of liver disease, and different treatment regimens. A recently published large-scale study on HBV/HCV coinfected patients demonstrated that high rates of sustained virological response (SVR) can be achieved in genotype 1 (73%) and 2/3 (86%) patients by Peg-IFN plus ribavirin,23 and there NVP-AUY922 solubility dmso was no significant differences in SVR between monoinfected HCV and coinfected HBV/HCV patients. Because the HBV DNA level in occult HBV is relatively lower than overt HBV/HCV coinfected patients, based on this, it might be reasonable to expect that low

levels of HBV should not have a major impact on treatment response. The severity of liver disease at the initiation of antiviral therapy, however, might be more important for determining ultimate antiviral efficacy. Montelukast Sodium To date, there is insufficient evidence to support the routine checking for HBV DNA by a PCR-based assay in CHC patients before the initiation of antiviral therapy, even in patients with serological markers of resolved HBV infection. Although undetectable HBV DNA can be achieved in a proportion of patients, the phenomenon of reciprocal viral interference of HBV and HCV can develop during or after antiviral therapy and result in the reappearance of serum

HBV DNA.23 Therefore, the possibility of occult HBV infection in CHC patients should be cautiously excluded especially during unexplained transaminase elevation despite a negative HCV RNA test found on repeat testing before or after antiviral therapy. In summary, occult HBV infection is a clinical entity characterized by the detection of HBV-DNA in serum, PBMC or liver in the absence of HBsAg. Occult HBV infection is more common in patients with CHC and has been described not only in patients who have resolved HBV infection but also in patients without any serological markers of HBV. The long-lasting persistence of HBV in the liver could provoke very mild but continuing necroinflammation that may contribute over time to the progression of the chronic liver damage towards cirrhosis if other causes of liver damage, such as CHC, co-exist.

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