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Spontaneous reactivation of hepatitis B virus replication in an HIV coinfected patient with isolated anti-Hepatitis B core antibodies.

ABSTRACT: Co-infections with HBV (hepatitis B virus) occur in HIV (human immunodeficiency virus) patients frequently. It has been reported that an effective treatment of HIV can also lead to a suppression of HBV and to anti-HBs seroconversion in HBV-infected patients. Here, we report a spontaneous reactivation of HBV replication in an HIV-infected patient with anti-HBc as the only marker of chronic HBV infection. The patient was known to be coinfected with HIV and HBV for years and the HBV DNA was measured repeatedly at low levels. A significant increase of HBV DNA up to 1.7 x 10? IU/ml was found accompanied with clinical symptoms of hepatitis. Multiple mutations occurred in the S gene during the flare-up of HBV as shown by sequencing, including I103T, K122R, M133I, F134V, D144E, V164E and L175S. Anti-HIV/HBV treatment led to a resolution of symptoms and to a decrease in the HIV RNA and HBV DNA viral load. It is possible that the accumulated mutations during HBV replication were selected and responsible for the reactivation.

SUBMITTER: Pei R

PROVIDER: S-EPMC3902409 | biostudies-literature | 2014

REPOSITORIES: biostudies-literature

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Spontaneous reactivation of hepatitis B virus replication in an HIV coinfected patient with isolated anti-Hepatitis B core antibodies.

Pei Rongjuan R Grund Sebastian S Verheyen Jens J Esser Stefan S Chen Xinwen X Lu Mengji M

Virology journal 20140121

Co-infections with HBV (hepatitis B virus) occur in HIV (human immunodeficiency virus) patients frequently. It has been reported that an effective treatment of HIV can also lead to a suppression of HBV and to anti-HBs seroconversion in HBV-infected patients. Here, we report a spontaneous reactivation of HBV replication in an HIV-infected patient with anti-HBc as the only marker of chronic HBV infection. The patient was known to be coinfected with HIV and HBV for years and the HBV DNA was measure ...[more]

PMID: 24444423

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Project description:BackgroundQuantitative hepatitis B core-related antigen (qHBcrAg) or antihepatitis B core antibody (qAnti-HBc) could be useful in monitoring liver fibrosis evolution during chronic hepatitis B virus (HBV) infection, yet it has not been assessed in human immunodeficiency virus (HIV)-HBV-coinfected patients undergoing treatment with tenofovir (TDF).MethodsOne hundred fifty-four HIV-HBV-infected patients initiating a TDF-containing antiretroviral regimen were prospectively followed. The qHBcrAg and qAnti-HBc and liver fibrosis assessment were collected every 6-12 months during TDF. Hazard ratios (HRs) assessing the association between qHBcrAg/qAnti-HBc and transitions from none/mild/significant fibrosis to advanced fibrosis/cirrhosis (progression) and from advanced fibrosis/cirrhosis to none/mild/significant fibrosis (regression) were estimated using a time-homogeneous Markov model.ResultsAt baseline, advanced liver fibrosis/cirrhosis was observed in 40 (26%) patients. During a median follow-up of 48 months (interquartile range, 31-90), 38 transitions of progression (IR = 7/100 person-years) and 34 transitions of regression (IR = 6/100 person-years) were observed. Baseline levels of qHBcrAg and qAnti-HBc were not associated with liver fibrosis progression (adjusted-HR per log10 U/mL = 1.07, 95% confidence interval [CI] = 0.93-1.24; adjusted-HR per log10 Paul-Ehrlich-Institute [PEI] U/mL = 0.85, 95% CI = 0.70-1.04, respectively) or regression (adjusted-HR per log10 U/mL = 1.17, 95% CI = 0.95-1.46; adjusted-HR per log10 PEI U/mL = 0.97, 95% CI = 0.78-1.22, respectively) after adjusting for age, gender, duration of antiretroviral therapy, protease inhibitor-containing antiretroviral therapy, and CD4+/CD8+ ratio. Nevertheless, changes from the previous visit of qAnti-HBc levels were associated with liver fibrosis regression (adjusted-HR per log10 PEIU/mL change = 5.46, 95% CI = 1.56-19.16).ConclusionsBaseline qHBcrAg and qAnti-HBc levels are not associated with liver fibrosis evolution in TDF-treated HIV-HBV coinfected patients. The link between changes in qAnti-HBc levels during follow-up and liver fibrosis regression merits further study.

Project description:Hepatitis B virus (HBV) core protein (HBc) contains an N-terminal domain (NTD, assembly domain) and a C-terminal domain (CTD), which are linked by a flexible linker region. HBc plays multiple essential roles in viral replication, including capsid assembly, packaging of the viral pregenomic RNA (pgRNA) into nucleocapsids, viral reverse transcription that converts pgRNA to the genomic DNA, and secretion of DNA-containing (complete) virions or genome-free (empty) virions. The HBc linker is generally assumed to act merely as a spacer between NTD and CTD but some results suggest that the linker may affect NTD assembly. To determine its role in viral replication, we have made a number of deletion and substitution mutants in the linker region, in either the presence or absence of CTD, and tested their abilities to support capsid assembly and viral replication in human cells. Our results indicate that the linker could indeed impede NTD assembly in the absence of CTD, which could be partially relieved by partial linker deletion. In contrast, when CTD was present, the linker deletions or substitutions did not affect capsid assembly. Deletion of the entire linker or its C-terminal part resulted in a partial defect in pgRNA packaging and severely impaired viral DNA synthesis. In contrast, deletion of the N-terminal part of the linker, or substitutions of the linker sequence, had little to no effect on RNA packaging or first-strand DNA synthesis. However, the N-terminal linker deletion and two linker substitution mutants were defective in the production of mature double-stranded viral DNA. Secretion of empty virions was blocked by all the linker deletions and substitutions tested. In particular, a conservative linker substitution that allowed mature viral DNA synthesis and secretion of complete virions severely impaired the secretion of empty virions, thus increasing the ratio of complete to empty virions that were secreted. Together, these results demonstrate that the HBc linker region plays critical and complex roles at multiple stages of HBV replication.

Project description:Hepatitis B virus (HBV) reactivation may occur with high risk immunosuppression, such as anti-cluster of differentiation (CD)20 antibodies (Abs). Appropriate HBV prophylaxis during anti-CD20 Ab therapy averts hepatitis, chemotherapy disruption, and death. Serologic evidence of prior HBV exposure is present in one in nine veterans in the Veterans Health Administration (VHA). In 2014, most (61%-73%) patients in the VHA who were receiving anti-CD20 Ab treatment underwent HBV testing, yet <20% of eligible patients received HBV antiviral prophylaxis. We aimed to prevent HBV reactivation by increasing HBV testing and antiviral treatment rates among anti-CD20 Ab recipients through prospective interventions. A multidisciplinary team of clinicians, pharmacists, and public health professionals developed comprehensive prevention systems, including national seminars/newsletters/websites; pharmacy criteria for HBV screening/treatment prior to anti-CD20 Ab use; changes to national formulary restrictions to expand HBV prophylaxis prescribing authority; Medication Use Evaluation Tracker to identify omissions; national e-mail alert to all VHA oncology providers detailing specific testing and HBV antiviral treatment needs; and a voluntary electronic medical record "order check" used at interested facilities (n = 11) to automatically assess pretreatment HBV testing and antiviral treatment and only generate a reminder to address deficiencies. Analysis of monthly data from June 2016 through September 2017 among anti-CD20 Ab recipients revealed pre-anti-CD20 Ab treatment HBV testing increased to 91%-96% and appropriate HBV antiviral prophylaxis to 76%-85% nationally following implementation of the intervention. Medical centers using the voluntary electronic medical record order check increased HBV testing rates to 93%-98% and HBV antiviral prophylaxis rates to 99%. Conclusion: Multimodal intervention systems to prevent HBV reactivation among VHA patients receiving anti-CD20 Ab therapies increased national rates of HBV testing to >90% and antiviral prophylaxis to >80%.

Dataset Information

Spontaneous reactivation of hepatitis B virus replication in an HIV coinfected patient with isolated anti-Hepatitis B core antibodies.

Publications

Spontaneous reactivation of hepatitis B virus replication in an HIV coinfected patient with isolated anti-Hepatitis B core antibodies.

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