Hepatocarcinoma in HBV infection is controlled by the use of entecavir, interferon and tenofovir: viral suppression and restoration of hepatic decompensation

Abstract

Objective: To elucidate how therapies with interferons and nucleotide analogues in patients infected with hepatitis B virus cause reversal of liver cirrhosis and hepatocarcinoma. Literature review: Entecavir has demonstrated virological and biochemical benefits, reducing the incidence of drug-resistant mutations, and being associated with a lower risk of death. Interferons (IFNs) have been used to treat chronic hepatitis B/C, IFNs induce APOBEC3G expression with activation of STAT3 inhibiting HBV, complexes of these IFNs activate the Janus-activated kinase signal transducer (JAK) and the transcription pathway activator (STAT), leading to the expression of IFN-stimulated genes (ISGs). Studies with tenofovir for hepatitis B suggest that it reverses hepatic fibrosis, tenofovir is hydrolysed by intestinal and plasma esterases, and is metabolized mainly intracellularly by cathepsin A. Final considerations: IFNs activate immune cells responsible for the antiviral response, entecavir acts as the HBV DNA strand terminator, and tenofovir is associated with reversal of liver fibrosis and restoration of kidney function.