BACKGROUND: The course of chronic HBV infection is modified by HIV-coexistence. OBJECTIVE: To analyze the role of HBV genomic heterogeneity in basal core promoter (BCP) and precore (Pc) genomic regions. STUDY DESIGN: In a 3-yr prospective study, 39 HBV infected patients (20 monoinfected and 19 HIV-coinfected) were included. Eighty-two HBV isolates were studied at quasispecies level in the BCP/Pc genomic region. Clinical records obtained include data on lamivudine therapy and resistance mutations, HBV and HIV-viral load. RESULTS: HBV isolates were predominantly ascribed to genotype (Gt) A2 among HBV-monoinfected and HIV-coinfected patients. BCP mutations in isolates from monoinfected patients were significantly more frequent than in those from coinfected ones, irrespective of the HBe expression pattern (p<0.0001). Regardless of the HIV-coexistence, the Pc mutation at G1896A only barely appeared among clone-derived sequences of GtF1 isolates, mainly from HBe(-) HBV-monoinfected patients. CONCLUSIONS: HBV isolates characterized from HIV-coinfected patients seem to be more prone to exhibit a wild type genomic pattern at BCP regulatory region with respect to those from HBV-monoinfected ones. Besides, mutations at Pc region might be genotype-dependent in their frequency but not on HIV co-presence related.
BACKGROUND: The course of chronic HBV infection is modified by HIV-coexistence. OBJECTIVE: To analyze the role of HBV genomic heterogeneity in basal core promoter (BCP) and precore (Pc) genomic regions. STUDY DESIGN: In a 3-yr prospective study, 39 HBV infectedpatients (20 monoinfected and 19 HIV-coinfected) were included. Eighty-two HBV isolates were studied at quasispecies level in the BCP/Pc genomic region. Clinical records obtained include data on lamivudine therapy and resistance mutations, HBV and HIV-viral load. RESULTS: HBV isolates were predominantly ascribed to genotype (Gt) A2 among HBV-monoinfected and HIV-coinfectedpatients. BCP mutations in isolates from monoinfected patients were significantly more frequent than in those from coinfected ones, irrespective of the HBe expression pattern (p<0.0001). Regardless of the HIV-coexistence, the Pc mutation at G1896A only barely appeared among clone-derived sequences of GtF1 isolates, mainly from HBe(-) HBV-monoinfected patients. CONCLUSIONS: HBV isolates characterized from HIV-coinfectedpatients seem to be more prone to exhibit a wild type genomic pattern at BCP regulatory region with respect to those from HBV-monoinfected ones. Besides, mutations at Pc region might be genotype-dependent in their frequency but not on HIV co-presence related.
Authors: Jennifer Grant; Oche Agbaji; Anna Kramvis; Mukhlid Yousif; Mu'azu Auwal; Sudhir Penugonda; Placid Ugoagwu; Robert Murphy; Claudia Hawkins Journal: Trop Med Int Health Date: 2017-05-22 Impact factor: 2.622
Authors: Sumathi Ramachandran; Xiangjun Zhai; Hong Thai; Davis S Campo; Guoliang Xia; Lilia M Ganova-Raeva; Jan Drobeniuc; Yury E Khudyakov Journal: PLoS One Date: 2011-09-20 Impact factor: 3.240