Treatment of Chronic Hepatitis B or C in HIV‐Infected Patients with Dual Viral Hepatitis

Soriano, Vincent; Barreiro, Pablo; Martín‐Carbonero, Luz; Castellares, Carol; Ruiz-Sancho, Andrés; Labarga, Pablo; Ramos, Belén; González-Lahoz, Juan

doi:10.1086/512679

Cited by 35 publications

(13 citation statements)

References 13 publications

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“…Similar to other studies, a high proportion (77%) of patients were infected with HBV/A [Soriano et al, 2007]. In a previous study, 33 patients infected with HIV/HBV were genotyped by sequence analysis of the S, pre‐S2, and partial pre‐S1 region.…”

Section: Discussionsupporting

confidence: 72%

Hepatitis B virus genotype G: Prevalence and impact in patients co‐infected with human immunodeficiency virus

Dao

Attar

Neak

et al. 2011

Journal of Medical Virology

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Relatively little is known about the role of hepatitis B virus (HBV) genotype G (HBV/G) in patients co-infected with human immunodeficiency virus (HIV) and HBV. This study examined the prevalence and association of HBV/G to liver fibrosis in co-infected patients. HBV genotypes were determined by direct sequencing of the HBV surface gene or Trugene® HBV 1.0 assay in 133 patients infected with HIV/HBV. Quantitative testing of HBV-DNA, HBeAg, and anti-HBe were performed using the Versant® HBV 3.0 (for DNA) and the ADVIA®Centaur assay. The non-invasive biomarkers Fib-4 and APRI were used to assess fibrosis stage. Genotype A was present in 103/133 (77%) of the cohort, genotype G in 18/133 (14%) with genotypes D in 8/133, (6%), F 2/133 (1.5%), and H 2/133 (1.5%). Genotype G was associated with hepatitis B e antigen-positivity and high HBV-DNA levels. Additionally, HBV/G (OR 8.25, 95% CI 2.3-29.6, P = 0.0012) was associated with advanced fibrosis score using Fib-4, whereas, being black was not (OR 0.19, 95% CI 0.05-0.07, P = 0.01). HBV/G in this population exhibited a different phenotype than expected for pure G genotypes raising the question of recombination or mixed infections. The frequent finding of HBV/G in co-infected patients and its association with more advanced fibrosis, suggests that this genotype leads to more rapid liver disease progression. Further studies are needed to understand why this genotype occurs more frequently and what impact it has on liver disease progression in patients with HBV/HIV.

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Section: Discussionsupporting

confidence: 72%

Hepatitis B virus genotype G: Prevalence and impact in patients co‐infected with human immunodeficiency virus

Dao

Attar

Neak

et al. 2011

Journal of Medical Virology

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“…We also report the first longitudinal data on the impact of treatment on both chronic hepatitis replication and HIV. Over an average follow‐up of 33 months per patient, co‐infection with HDV and/or HCV, low HIV viral load, higher CD4 counts and concurrent treatment with adefovir or tenofovir stood as independent determinants of HBV‐DNA undetectability, confirming cross‐sectional or retrospective data on the subject [1,21–28]. Co‐infection with HDV emerged as a determinant of HCV‐RNA undetectability, yet not statistically significant, considering the small number of patients in the quad‐infected group ( n = 12).…”

Section: Discussionmentioning

confidence: 76%

Longitudinal evaluation of viral interactions in treated HIV-hepatitis B co-infected patients with additional hepatitis C and D virus

Boyd

Lacombe

Miailhes

et al. 2010

Journal of Viral Hepatitis

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Virological interactions of hepatitis B (HBV), hepatitis C (HCV) and hepatitis D (HDV) viruses in HIV-infected patients have been poorly characterized especially under treatment influences. Undetection rates of hepatitis viruses were longitudinally analyzed in a 3-year cohort of 308 HIV-HBV co-infected patients and compared using Generalized Estimating Equation models adjusted for age, HIV-RNA, CD4 cell-count and antiviral treatment. Chronic hepatitis co-infection in HIV-infected patients (age years, SD) was: 265 HBV (40.7, 8.2); 19 HBV-HCV (39.7, 4.1); 12 HBV-HDV (35.2, 9.9); 12 HBV-HCV-HDV (39.2, 5.2). At inclusion, treatment with lamivudine/tenofovir was not significantly different between co-infection groups. HBV suppression was significantly associated with HDV (aOR = 3.85, 95%CI 1.13-13.10, P = 0.03) and HCV tri-infection (aOR = 2.65, 95%CI 1.03-6.81, P = 0.04), but marginally associated with HIV-HBV-HCV-HDV (aOR = 2.32, 95%CI 0.94-5.74, P = 0.07). In quad-infection, lower HDV-undetectability (vs HIV-HBV-HDV, P = 0.2) and higher HCV-undetectability (vs HIV-HBV-HCV, P = 0.1) were demonstrated. The degree of HBV suppression varied between visits and co-infection groups [range of aOR during follow-up (vs HIV-HBV co-infection): HIV-HBV-HCV = 2.23-5.67, HIV-HBV-HDV = 1.53-15.17]. In treated co-infected patients, HDV expressed continuous suppression over HCV- and HBV-replications. Peaks and rebounds from undetectable hepatitis B, C and/or D viremia warrant closer follow-up in this patient population. HDV-replication was uncontrolled even with antiviral treatment.

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“…HCV co‐infection was present in 42% of our HIV‐ and HBV‐infected patients. Generally, replication of one virus predominates over the other because of a reciprocal inhibitory effect [17]. At this point, the molecular mechanism(s) of reciprocal replicative suppression in HBV–HCV co‐infection are unknown.…”

Section: Discussionmentioning

confidence: 99%

Liver enzyme elevation after lamivudine withdrawal in HIV–hepatitis B virus co‐infected patients: the Swiss HIV Cohort Study

Bellini

Keiser

et al. 2008

HIV Medicine

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Background The principal causes of liver enzyme elevation among HIV–hepatitis B virus (HBV) co‐infected patients are the hepatotoxic effects of antiretroviral therapy (ART), alcohol abuse, ART‐induced immune reconstitution and the exacerbation of chronic HBV infection. Objectives To investigate the incidence and severity of liver enzyme elevation, liver failure and death following lamivudine (3TC) withdrawal in HIV–HBV co‐infected patients. Methods Retrospective analysis of the Swiss HIV Cohort Study database to assess the clinical and biological consequences of the discontinuation of 3TC. Variables considered for analysis included liver enzyme, HIV virological and immunological parameters, and medication prescribed during a 6‐month period following 3TC withdrawal. Results 3TC was discontinued in 255 patients on 363 occasions. On 147 occasions (109 patients), a follow‐up visit within 6 months following 3TC withdrawal was recorded. Among these patients, liver enzyme elevation occurred on 42 occasions (29%), three of them (2%) with severity grade III and five of them (3.4%) with severity grade IV elevations (as defined by the AIDS Clinical Trials Group). Three patients presented with fulminant hepatitis. One death (0.7%) was recorded. Conclusions HBV reactivation leading to liver dysfunction may be an under‐reported consequence of 3TC withdrawal in HIV–HBV co‐infected patients. Regular monitoring of HBV markers is warranted if active therapy against HBV is discontinued.

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Treatment of Chronic Hepatitis B or C in HIV‐Infected Patients with Dual Viral Hepatitis

Cited by 35 publications

References 13 publications

Hepatitis B virus genotype G: Prevalence and impact in patients co‐infected with human immunodeficiency virus

Hepatitis B virus genotype G: Prevalence and impact in patients co‐infected with human immunodeficiency virus

Longitudinal evaluation of viral interactions in treated HIV-hepatitis B co-infected patients with additional hepatitis C and D virus

Liver enzyme elevation after lamivudine withdrawal in HIV–hepatitis B virus co‐infected patients: the Swiss HIV Cohort Study

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