Analysis of hepatocellular carcinoma associated with hepatitis B virus

Abstract

The hepatitis B virus (HBV) is considered one of the main driving forces in the development of hepatocellular carcinoma (HCC). Human HBV is a partially double-stranded DNA (dsDNA) virus consisting of approximately 3.2 kbp. HBV predominantly infects hepatocytes via the receptor sodium taurocholate cotransporting polypeptide (NTCP) and coreceptor hepatic proteoglycan. The replication of HBV in hepatocytes leads to apoptosis while simultaneously leading to cirrhosis and cancer. Although the integration of dsDNA into the hepatocyte genome seems to be the main cause of mutation, since the discovery of their function, viral proteins have been shown to regulate the P53 pathway or P13K/AKT pathway to prevent host cell apoptosis, causing uncontrolled proliferation of liver cells leading to the formation of solid tumours. The most common treatments involve nucleo(s)tide analogue (NA) and polyethylene glycol (PEG)ylated interferon-alpha (PegIFN-α). NA treatment has been found to be effective for the majority of patients and induces few side effects. Nevertheless, the rate of seroconversion is relatively low. PegIFN treatment is contraindicated during pregnancy and leads to a higher morbidity rate, but the seroconversion rate is high. Since medicines and vaccines have been developed, the incidence and mortality of HBV related to HCC have profoundly decreased compared to those in 2000. This review investigates what can be the potential mechanism that HBV can cause HBV and the treatment used in chronic and acute infection.