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Hepatitis B virus (HBV) infection is one of the most complex and fascinating viral infections. The resolution of HBV infection is shown by the disappearance of HBV DNA from serum, by hepatitis e and hepatitis B surface antigen (HBsAg) seroconversion, and by a full normalisation of liver transaminases. These biological laboratory tests should characterise a full clearance of the virus. This is not the case with HBV. The complexity of the infection resides in the very long immunological response that can continue for years, after the acute phase, and as demonstrated by several studies by the positivity of HBV DNA in serum, peripheral mononuclear cells and liver, years after the apparent recovery.1 Therefore, only the absence of DNA in the liver means a cure. Even though there are no clear-cut data showing that low levels of HBV DNA can cause a progression of liver damage, it is pretty clear that either spontaneously or after immunesuppressive therapy, HBV can reactivate (rHBV).2 3 Once HBV DNA still is detectable, yet there is no detectable HBsAg, the biology claims there is occult hepatitis B virus infection (OBI). OBI is defined as the presence of replication-competent HBV DNA (ie, episomal HBV covalently closed circular DNA (cccDNA) in the blood and/or in the liver of people who test negative for HBsAg by currently available assays.4 5 It has been demonstrated that HBV DNA is only intermittently detected in serum/plasma, and when detectable, the concentration is low, usually less than 200 IU/mL (about 1000 copies/mL).6 From a molecular point of view, OBI is characterised by the stability and long-term persistence of cccDNA in the nucleus of infected hepatocytes, with a strong suppression of overall replication activity and viral protein expression exerted by the host’s defence mechanisms. The presence of replication-competent HBV DNA and …
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