Patterns and Causes of Suboptimal Response to Tenofovir-Based Therapy in Individuals Coinfected With HIV and Hepatitis B Virus

Matthews, Gail V.; Avihingsanon, Anchalee; Bowden, Scott; Dore, Gregory J.; Lewin, Sharon R.; Sasadeusz, Joe; Revill, Peter; Hoy, Jennifer; Finlayson, Robert; Ruxrungtham, Kiat; Saulynas, Melissa; Locarnini, Stephen; Thio, Chloe L.

doi:10.1093/cid/cit002

Cited by 73 publications

(66 citation statements)

References 14 publications

(20 reference statements)

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“…Baseline CD4 + T cells were significantly associated with HBV DNA suppression at 12 months but not at other visits. This concurs with other studies such as Kim et al [43] who reported baseline CD4 + T cells as a predictor of HBV suppression in response to tenofovir [44]. …”

Section: Discussionsupporting

confidence: 93%

Slow CD4+ T-Cell Recovery in Human Immunodeficiency Virus/Hepatitis B Virus-Coinfected Patients Initiating Truvada-Based Combination Antiretroviral Therapy in Botswana

Anderson

Gaseitsiwe

Moyo

et al. 2016

Open Forum Infectious Diseases

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Background. Hepatitis B virus (HBV) and human immunodeficiency virus (HIV) coinfection has emerged as an important cause of morbidity and mortality. We determined the response to Truvada-based first-line combination antiretroviral therapy (cART) in HIV/HBV-coinfected verus HIV-monoinfected patients in Botswana.Methods. Hepatitis B virus surface antigen (HBsAg), HBV e antigen (HBeAg), and HBV deoxyribonucleic acid (DNA) load were determined from baseline and follow-up visits in a longitudinal cART cohort of Truvada-based regimen. We assessed predictors of HBV serostatus and viral suppression (undetectable HBV DNA) using logistic regression techniques.Results. Of 300 participants, 28 were HBsAg positive, giving an HIV/HBV prevalence of 9.3% (95% confidence interval [CI], 6.3–13.2), and 5 of these, 17.9% (95% CI, 6.1–36.9), were HBeAg positive. There was a reduced CD4+ T-cell gain in HIV/HBV-coinfected compared with HIV-monoinfected patients. Hepatitis B virus surface antigen and HBeAg loss was 38% and 60%, respectively, at 24 months post-cART initiation. The HBV DNA suppression rates increased with time on cART from 54% to 75% in 6 and 24 months, respectively.Conclusions. Human immunodeficiency virus/HBV coinfection negatively affected immunologic recovery compared with HIV-1C monoinfection. Hepatitis B virus screening before cART initiation could help improve HBV/HIV treatment outcomes and help determine treatment options when there is a need to switch regimens.

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Section: Discussionsupporting

confidence: 93%

Slow CD4+ T-Cell Recovery in Human Immunodeficiency Virus/Hepatitis B Virus-Coinfected Patients Initiating Truvada-Based Combination Antiretroviral Therapy in Botswana

Anderson

Gaseitsiwe

Moyo

et al. 2016

Open Forum Infectious Diseases

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“…We also found that drug-resistant HBV only emerged in those on lamivudine or emtricitabine monotherapy, which is consistent with data showing no resistance with TDF-based therapy [22, 28, 29]. …”

Section: Discussionsupporting

confidence: 90%

Comparison of HBV-active HAART regimens in an HIV–HBV multinational cohort

Thio

Smeaton

Hollabaugh

et al. 2015

Aids

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Objectives To explore factors associated with short and long-term HBV DNA suppression in a multinational cohort of HIV-HBV co-infected subjects receiving HBV-active antiretrovirals. Methods 115 HIV-HBV co-infected subjects participating in one of two global ACTG randomized clinical trials of different antiretroviral regimens received either HBV-monotherapy with either lamivudine or emtricitabine (N=56) or HBV-dual therapy with TDF plus lamivudine or emtricitabine (N=59). Associations of pre-treatment characteristics with the primary (HBV DNA <200 IU/ml at 24 weeks) and longitudinal outcomes through 144 weeks were explored using logistic regression. HBV drug-resistance mutations were determined by pol sequencing in those with viral rebound. Results The proportion with HBV DNA<200 IU/ml was 60% (95% CI 50%–69%) at 24 weeks and 79% (95% CI 69%–88%) at 144 weeks. Pre-treatment factors associated with the primary outcome were HBV DNA, CD4 T-cell count, and AST, but only pre-treatment HBV DNA remained associated with long-term suppression (P<0.0001). HBV therapy group was not significantly associated with the primary outcome at 24 weeks; however, longitudinally, a greater proportion in the dual therapy group achieved HBV DNA<200 IU/mL (P=0.007). A higher proportion of hepatitis B e antigen negative subjects (n=57) achieved HBV DNA <200 IU/ml at any point, regardless of therapy group. All 12 subjects with emergence of lamivudine-resistant mutants were in the monotherapy group. Conclusions TDF-based dual HBV-active antiretroviral therapy is preferred to treat HIV-HBV co-infected patients. In resource-limited settings where TDF may not be universally available, lamivudine or emtricitabine HBV-monotherapy is a reasonable option in patients with low HBV replication.

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“…No other anti-HBV agents were associated with intrahepatic viral loads with the exception of significantly higher total IH-DNA in univariable analysis after 3-6 years of cumulative LAM-exposure, most likely due to the presence of LAM-resistance. These observations bolster previous works among HIV-HBV co-infected patients where similar conclusions were reached using plasma HBV-DNA levels [18][19][20]. Nevertheless, the data presented here allow a more thorough understanding of how these factors are associated with activity in the liver, which is not necessarily the case when measuring circulating HBV-DNA levels [21].…”

Section: Discussionsupporting

confidence: 86%

Decay of ccc-DNA marks persistence of intrahepatic viral DNA synthesis under tenofovir in HIV-HBV co-infected patients

Boyd

Lacombe

Lavocat

et al. 2016

Journal of Hepatology

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Patterns and Causes of Suboptimal Response to Tenofovir-Based Therapy in Individuals Coinfected With HIV and Hepatitis B Virus

Abstract: Tenofovir/emtricitabine was superior to other anti-HBV regimens in long-term HBV suppression. HBV viremia on therapy was identified in 1 of 3 main patterns. Suboptimal adherence was associated with detectable HBV DNA during therapy, even when HIV was undetectable.

Cited by 73 publications

References 14 publications

Slow CD4+ T-Cell Recovery in Human Immunodeficiency Virus/Hepatitis B Virus-Coinfected Patients Initiating Truvada-Based Combination Antiretroviral Therapy in Botswana

Slow CD4+ T-Cell Recovery in Human Immunodeficiency Virus/Hepatitis B Virus-Coinfected Patients Initiating Truvada-Based Combination Antiretroviral Therapy in Botswana

Comparison of HBV-active HAART regimens in an HIV–HBV multinational cohort

Decay of ccc-DNA marks persistence of intrahepatic viral DNA synthesis under tenofovir in HIV-HBV co-infected patients

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