BACKGROUND AND STUDY AIMS: Recent findings introduced APOBEC3G (A3G) as a host factor that blocks viral replication. It induces G to A hypermutations in viral DNA at the step of reverse transcription and in response to interferon. This study aimed to investigate the expression of liver A3G protein in association with both replication of hepatitis B virus (HBV) and frequency of G to A mutations in BCP (basal core promoter)-PC (pre-core) region. PATIENTS AND METHODS: Fifty-one liver biopsies of naïve chronic hepatitis B (CHB) patients enrolled for the expression of A3G were done by immunohistochemistry (IHC) standard method. The presence of HBV DNA and sequences of BCP-PC region at the time of liver biopsy was investigated in all patients. RESULTS: Among 34 patients with detectable HBV DNA, 31 carried 1-5 G to A mutations in the BCP-PC region. IHC results showed that the expression level of A3G in CHB patients' liver was very low. Of all patients, A3G is expressed in three undetectable HBV DNA subjects and a patient with 2.24×10(4) copies ml(-1) of HBV DNA. G to A mutated residues were indicated at positions 1727, 1757 and 1896 of the HBV genome of this patient. CONCLUSION: This study indicates that despite very low levels of both A3G in liver and the number of positive subjects, A3G has a potential role to restrict the in vivo replication of HBV.
BACKGROUND AND STUDY AIMS: Recent findings introduced APOBEC3G (A3G) as a host factor that blocks viral replication. It induces G to A hypermutations in viral DNA at the step of reverse transcription and in response to interferon. This study aimed to investigate the expression of liver A3G protein in association with both replication of hepatitis B virus (HBV) and frequency of G to A mutations in BCP (basal core promoter)-PC (pre-core) region. PATIENTS AND METHODS: Fifty-one liver biopsies of naïve chronic hepatitis B (CHB) patients enrolled for the expression of A3G were done by immunohistochemistry (IHC) standard method. The presence of HBV DNA and sequences of BCP-PC region at the time of liver biopsy was investigated in all patients. RESULTS: Among 34 patients with detectable HBV DNA, 31 carried 1-5 G to A mutations in the BCP-PC region. IHC results showed that the expression level of A3G in CHB patients' liver was very low. Of all patients, A3G is expressed in three undetectable HBV DNA subjects and a patient with 2.24×10(4) copies ml(-1) of HBV DNA. G to A mutated residues were indicated at positions 1727, 1757 and 1896 of the HBV genome of this patient. CONCLUSION: This study indicates that despite very low levels of both A3G in liver and the number of positive subjects, A3G has a potential role to restrict the in vivo replication of HBV.