JIA-HORNG KAO2021-09-042021-09-0420071386-6346https://www.scopus.com/inward/record.uri?eid=2-s2.0-34447632856&doi=10.1111%2fj.1872-034X.2007.00105.x&partnerID=40&md5=9033a3cbd871dc226777f7e83ff87a78https://scholars.lib.ntu.edu.tw/handle/123456789/582159Hepatitis B is not only a preventable but now treatable disease. Five drugs have been approved for the treatment of chronic hepatitis B virus (HBV) infection: standard interferon-α (IFN), pegylated IFN, lamivudine, adefovir dipivoxil and entecavir. Among these agents, the responses to interferon therapy are invariably influenced by both host and viral factors. Therefore, understanding these factors is important for practicing hepatologists, and it may help design individualized medicine for the treatment of chronic hepatitis B. HBV genotypes affect the disease progression and outcomes of HBV-related chronic liver disease, as well as the response to antiviral treatments. Existing data indicate a better sustained response to standard IFN-α in HBeAg positive genotype B patients than genotype C patients, and in genotype A patients than genotype D patients. Nevertheless, conflicting results exist regarding the response to pegylated IFN, and more studies are needed. As to HBV genetic polymorphisms, a recent study showed that an IFN sensitivity-determiningregion may not exist within the whole genome of HBV subgenotype Ba, and host factors as well as virus-host interactions may be more important than viral factors alone in determining the treatment outcomes with IFN. Regarding host genetic polymorphisms, single nucleotide polymorphisms within eukaryotic translation initiation factor 2 and MxA promoter regions may be associated with the responsiveness to standard IFN-α treatment in patients with HBeAg positive chronic hepatitis B. In the foreseeable future, individualized chronic hepatitis B treatment algorithms should be tailored to host (immune status, ALT level and genomic polymorphisms), virus (HBeAg status, HBV DNA level, genotype, precore/ basal core promoter mutants and pre-S deletion mutant) as well as liver disease status (hepatitis activity and fibrosis stage). ? 2007 The Japan Society of Hepatology.Chronic hepatitis; Genotype; Hepatitis B virus; Interferon; Peginterferon; Ribavirin[SDGs]SDG3adefovir dipivoxil; alanine aminotransferase; alpha interferon; alpha2a interferon; entecavir; hepatitis B(e) antigen; interferon; lamivudine; Myxovirus resistance protein A; peginterferon; peginterferon alpha2a; peginterferon alpha2b; placebo; ribavirin; virus DNA; alanine aminotransferase blood level; anemia; chronic hepatitis; chronic liver disease; clinical trial; combination chemotherapy; conference paper; disease activity; disease association; disease course; drug absorption; drug blood level; drug distribution; drug efficacy; drug half life; drug mechanism; drug response; drug safety; drug tolerability; drug use; gene deletion; genetic algorithm; genetic code; genetic polymorphism; genotype; hepatitis B; Hepatitis B virus; human; liver fibrosis; monotherapy; nephrotoxicity; nonhuman; outcome assessment; priority journal; promoter region; sensitivity analysis; single nucleotide polymorphism; treatment duration; unspecified side effect; virus cell interaction; virus gene; virus genome; virus strainConference Paper10.1111/j.1872-034X.2007.00105.x2-s2.0-34447632856