13 research outputs found

    Functional Cure of Hepatitis B Virus Infection in Individuals With HIV-Coinfection: A Literature Review

    No full text
    International audienceIn individuals infected with hepatitis B virus (HBV), the loss of hepatitis B surface antigen (HBsAg) is the ultimate therapeutic goal, which defines “functional cure.” For individuals living with human immunodeficiency virus (HIV), functional cure occurs roughly 2 per 100 person-years during potent anti-HBV containing antiretroviral therapy. Although this rate may be higher than expected in treated HBV mono-infected individuals, rates of functional cure widely vary between studies (0.6–10.5 per 100 person-years). Similar to HBV mono-infection, the phase of HBV infection, HBV (sub-)genotypes and hepatitis B “e” Ag-negative variants are associated with functional cure in treated HIV-HBV co-infection. In specifically HIV-HBV co-infected individuals, strong increases in CD4+ T cell counts after treatment initiation have also been linked to functional cure, yet this finding is inconsistent across studies. Several markers directly or indirectly reflecting HBV activity are being developed to predict functional cure, such as quantification of HBsAg, hepatitis B core-related antigen, HBsAg protein composition, anti-hepatitis B core antibodies and interferon-gamma-inducible protein 10. Few have been assessed during treatment in HIV-HBV co-infected individuals and none have been validated to predict functional cure. Novel therapeutics for HBV cure are essential for individuals with HIV-HBV co-infection and need to be separately evaluated in this population

    Functional cure of hepatitis B virus infection in individuals with hiv-coinfection: A literature review

    No full text
    In individuals infected with hepatitis B virus (HBV), the loss of hepatitis B surface antigen (HBsAg) is the ultimate therapeutic goal, which defines “functional cure.” For individuals living with human immunodeficiency virus (HIV), functional cure occurs roughly 2 per 100 person-years during potent anti-HBV containing antiretroviral therapy. Although this rate may be higher than expected in treated HBV mono-infected individuals, rates of functional cure widely vary between studies (0.6–10.5 per 100 person-years). Similar to HBV mono-infection, the phase of HBV infection, HBV (sub-)genotypes and hepatitis B “e” Ag-negative variants are associated with functional cure in treated HIV-HBV co-infection. In specifically HIV-HBV co-infected individuals, strong increases in CD4+ T cell counts after treatment initiation have also been linked to functional cure, yet this finding is inconsistent across studies. Several markers directly or indirectly reflecting HBV activity are being developed to predict functional cure, such as quantification of HBsAg, hepatitis B core-related antigen, HBsAg protein composition, anti-hepatitis B core antibodies and interferon-gamma-inducible protein 10. Few have been assessed during treatment in HIV-HBV co-infected individuals and none have been validated to predict functional cure. Novel therapeutics for HBV cure are essential for individuals with HIV-HBV co-infection and need to be separately evaluated in this population

    Monitoramento de vírus respiratórios na região metropolitana de Belo Horizonte, 2011 a 2013

    No full text
    Resumo OBJETIVO: analisar a circulação dos vírus respiratórios em residentes na região metropolitana de Belo Horizonte, Brasil, hospitalizados em Belo Horizonte, de 2011 a 2013. MÉTODOS: estudo descritivo de 5.158 indivíduos com síndrome respiratória aguda grave; foram comparadas as características dos casos confirmados com casos descartados ou sem coleta de swab. RESULTADOS: metade dos vírus isolados foi da influenza A, especialmente os subtipos A(H1N1)pdm09 em pessoas de 20-59 anos e A(H3N2) naquelas com 60 anos ou mais; crianças menores de cinco anos tiveram identificado, com maior frequência, o vírus sincicial respiratório (65,6%), seguido pelo vírus da influenza A (21,2%); o vírus da influenza circulou em todas as estações do ano, e seus períodos de maior incidência intercalaram-se com os de maior atividade do vírus sincicial respiratório. CONCLUSÃO: o monitoramento dos vírus respiratórios contribui para o conhecimento dos períodos de circulação viral e a adoção de medidas de controle específicas

    ESTUDO DA MORTALIDADE E IMPACTO DAS INFECÇÕES POR HIV, HCV E HBV EM PORTADORES DE HEMOFILIA EM BELO HORIZONTE, 1985-2021

    No full text
    Introdução/Objetivo: Pacientes com hemofilia representam população com histórico de maior prevalência e mortalidade por infecções de transmissão parenteral. Avanços terapêuticos vêm aumentando a segurança transfusional e reduzindo o impacto dessas infecções na morbimortalidade. Os objetivos deste trabalho foram analisar a mortalidade geral em portadores de hemofilia assistidos no Hemocentro de Belo Horizonte (HBH), entre janeiro de 1985 e março de 2021, assim como suas causas e a ocorrência das infecções pelo HIV, HCV e HBV. Métodos: Coorte retrospectiva com portadores de hemofilia, sexo masculino, cadastrados no HBH entre janeiro de 1985 e dezembro de 2020, com pelo menos um retorno até 31/03/2021. A ocorrência de óbito (até 31/03/2021), suas causas, e variáveis sociodemográficas, epidemiológicas, clínicas e laboratoriais foram coletadas até março/2023 a partir de fontes secundárias (prontuários médicos, Sistema de Informação de Mortalidade-SIM e Webcoagulopatias). O estudo foi aprovado pelo Comitê de Ética em Pesquisa local. Resultados: Foram incluídos 870 pacientes com hemofilia: 715 do tipo A (82,2%) e 155 do tipo B (17,8%), sendo 446 (51,3%) classificados com hemofilia grave, 318 moderada (36,6%) e 106 leve (12,2%). Um total de 854 pacientes (98,2%) recebeu hemotransfusão ou hemoderivados no período: 394 (45,3%) usaram crioprecipitado, 360 (41,4%) concentrado de hemácias e 242 (27,8%) plasma fresco congelado em algum momento da vida. Apenas 323 (37,1%) fizeram uso exclusivo de hemoderivado industrializado. Em relação às sorologias no período, apresentaram positividade para anti-HCV: 258 (29,7%); anti-HIV-1/2: 80 (9,2%); anti-HBc-total: 188 (21,6%); e HBsAg: 13 (1,5%). Foram registrados 169 óbitos (19,4%) numa idade mediana de 32 anos. As causas mais frequentes de óbito foram: hemofilia/hemorragia em 73 (43,2%) pacientes, HIV/Aids em 48 (28,4%), sendo 39 deles (81,3%) entre os anos 1985 a 2000; e hepatopatia crônica em 19 (11,2%), sendo 15 deles (78,9%) ocorridos à partir do ano 2000. Conclusões: Os óbitos ocorreram precocemente nesta população, causados principalmente pela própria hemofilia/hemorragia, seguida pela infecção HIV/Aids nas décadas de 1980/1990 e as hepatopatias crônicas a partir dos anos 2000. O estudo indica a importância das comorbidades infecciosas transmissíveis pelo sangue na mortalidade desta população, com impactos diferenciados frente aos avanços terapêuticos e de biossegurança transfusionais alcançados ao longo do período

    Persistent HBV replication and serological response during up to 15 years of tenofovir-based antiretroviral therapy in HIV/HBV-coinfected patients: a multicentre prospective cohort study

    No full text
    International audienceObjectivesTo determine the extent of hepatitis B virus (HBV) suppression and its association with seroclearance of hepatitis ‘e’ antigen (HBeAg) and hepatitis B surface antigen (HBsAg) in HIV/HBV-coinfected patients undergoing long-term tenofovir-based antiretroviral therapy (ART).MethodsWe prospectively followed 165 HIV/HBV-coinfected patients undergoing tenofovir-based ART. Serum HBV-DNA viral loads and HBeAg and HBsAg status were obtained at tenofovir initiation and every 6–12 months. We calculated the proportion achieving virological response (VR, <60 IU/mL) during follow-up. We also calculated rates of HBeAg- and HBsAg-seroclearance, which were compared between those who achieved versus never achieved VR during follow-up using an Exact binomial test.ResultsDuring a median 8.1 years (IQR = 4.0–13.2) of tenofovir treatment, 152 (92.1%) patients were able to achieve VR and 13 (7.9%) never achieved VR (median HBV-DNA at the end of follow-up = 608 IU/mL, range = 67–52 400 000). The prevalence of individuals with detectable HBV-DNA (≥60 IU/mL) decreased during tenofovir treatment: 15.1% (n = 14/93) at 5 years, 3.2% (n = 2/62) at 10 years and, 3.2% (n = 1/31) at 15 years. 44/96 HBeAg-positive patients (6.15/100 person-years) had HBeAg-seroclearance and 13/165 patients overall (0.87/100 person-years) had HBsAg-seroclearance. No difference in HBeAg-seroclearance was observed between those who achieved versus never achieved VR (7.4 versus 3.7/100 person-years, P = 0.33), while HBsAg-seroclearance was only observed in those with VR (1.0 versus 0/100 person-years, P = 0.49; respectively). Individuals with VR also had a higher frequency of undetectable HIV-RNA during treatment (P < 0.001).ConclusionsDuring long-term tenofovir-based ART for HIV/HBV coinfection, persistent HBV viraemia is apparent, but becomes less frequent over time. HBsAg-seroclearance only occurred in those with full HBV and relatively high HIV suppression

    Profiles of liver fibrosis evolution during long-term tenofovir treatment in HIV-positive patients coinfected with hepatitis B Running title: Liver fibrosis evolution in HIV/HBV coinfection

    No full text
    International audienceBackground & AimsData on liver fibrosis evolution and its involvement in liver-related morbidity are scarce in individuals with human immunodeficiency virus (HIV) and hepatitis B virus (HBV) co-infection during treatment. We identified profiles of liver fibrosis evolution in coinfected patients undergoing tenofovir (TDF).MethodsWe included 169 HIV-HBV-coinfected patients on TDF-based antiretroviral therapy. Virological and clinical data were obtained at TDF-initiation and every 6-12 months. From data on non-invasive liver fibrosis assessments collected yearly (FibroTest®), we established clusters of individuals with similar liver fibrosis evolution using group-based trajectory models.ResultsFour profiles of liver fibrosis evolution were established from a median follow-up of 7.6 years (IQR = 3.1-13.1): low fibrosis with no progression (29.6%, profile A), low fibrosis with progression (22.5%, profile B), moderate fibrosis with high fluctuation (39.6%, profile C), and cirrhosis with no regression (8.3%, profile D). When compared to profile A, baseline HBeAg-positive status was associated with profiles B (P = .007) and C (P = .004), older age with profiles C (P < .001) and D (P = .001), exposure to second-generation protease inhibitors with profile C (P = .004), and CD4+ <500/mm3 at the last visit with profiles C (P = .02) and D (P = .002). Incident liver-related events occurred in profiles other than A (B, n = 1/38; C, n = 6/67; D, n = 3/14) and all five cases of hepatocellular carcinoma occurred in profiles C (n = 2) and D (n = 3).ConclusionsTDF-treated HIV-HBV coinfected individuals do not seem to benefit from comparable levels of liver fibrosis regression as in HBV mono-infection. Liver-related morbidity occurs mainly in those with fluctuating or consistently high fibrosis levels

    Effect of viral replication and liver fibrosis on all-cause mortality in HIV/HBV coinfected individuals: a retrospective analysis of a 15-year longitudinal cohort

    No full text
    International audienceBackground: In individuals co-infected with HIV and hepatitis B virus (HBV), widespread tenofovir (TDF)-containing antiretroviral therapy (ART) has led to substantial decreases in HBV-DNA and HIV-RNA detection. However, the link between viral replication, liver fibrosis, and mortality remains unclear.Methods: 300 HIV-HBV co-infected individuals undergoing ART were prospectively followed. Virological and clinical data were obtained at baseline and every 6-12 months. We quantified the association between HBV-DNA, HIV-RNA, and liver fibrosis with risk of all-cause mortality using a joint longitudinal-survival model. Viral detection, viral loads, and time-averaged cumulative viral loads of HIV and HBV were modeled as three separate exposures.Results:During a median 10.5 years (IQR=4.0-14.6), the proportion undergoing TDF-containing ART (baseline=18.7%, end of follow-up=79.1%) and with undetectable HBV-DNA (baseline=36.7%, end of follow-up=94.8%) substantially increased. HIV-RNA was mostly undetectable during follow-up (76.6%). 42 participants died (incidence rate=1.30/100person-years, 95%CI=0.96-1.76). The leading causes of death were non-AIDS/non-liver-related malignancies (28.6%), followed by liver-related (16.7%), AIDS-related (16.7%), and other (16.7%). All-cause mortality was associated with HBV-DNA viral load (adjusted-HR per log10IU/mL=1.41, 95%CI=1.04-1.93, p=0.03) or time-averaged cumulative HBV-DNA (adjusted-HR per log10IU-years=1.37, 95%CI=1.03-1.83, p=0.03), but not undetectable HBV-DNA (adjusted-HR=0.30, 95%CI=0.08-1.09, p=0.08). Advanced liver fibrosis at baseline was also associated with increased mortality rates (adjusted-HR=2.35, 95%CI=1.16-4.76, p=0.02). No significant association between HIV-RNA replication and mortality was observed.Conclusions: Concurrent and historical HBV replication and liver fibrosis are important drivers of all-cause mortality in largely TDF-treated HIV-HBV co-infected individuals, despite one-fifth of deaths being liver-related. HBV-DNA and liver fibrosis remain important prognostic indicators for this patient population

    Kinetics of Hepatitis B Core–Related Antigen and Anti–Hepatitis B Core Antibody and Their Association With Serological Response in Human Immunodeficiency Virus–Hepatitis B Coinfection

    No full text
    International audienceBackground: The aim of the current study was to describe the kinetics of quantified hepatitis B core-related antigen (qHBcrAg) and quantified anti-hepatitis B core antibody (qAnti-HBc) during tenofovir (TDF) treatment and assess their ability to predict hepatitis B e antigen (HBeAg) seroclearance in patients coinfected with human immunodeficiency virus (HIV) and hepatitis B virus.Methods: Serum qHBcrAg, qAnti-HBc, and hepatitis B virus DNA were obtained at TDF initiation and every 6-12 months. The on-treatment kinetics of qHBcrAg (ΔqHBcrAg) and qAnti-HBc (ΔqAnti-HBc) were estimated using mixed-effect linear regression. Hazard ratios (HRs) assessing the association between markers and HBeAg seroclearance were calculated using proportional hazards regression, and the sensitivity (Se) and specificity (Sp) of marker levels in predicting HBeAg seroclearance were assessed using time-dependent receiving operating characteristic curves.Results: During a median of 4.6 years, the cumulative incidences of hepatitis B surface antigen and HBeAg seroclearance were 3.2% (n = 5 of 158) and 27.4% (n = 26 of 95), respectively. ΔqHBcrAg was biphasic in HBeAg-positive patients (-0.051 and -0.011 log10 U/mL/mo during ≤18 and >18 months, respectively) and monophasic in HBeAg-negative patients. ΔqAnti-HBc was monophasic regardless of HBeAg status. In HBeAg-positive patients, baseline qHBcrAg and qAnti-HBc levels were associated with HBeAg seroclearance (adjusted HR, 0.48/log10 U/mL [95% confidence interval, .33-.70] and unadjusted HR, 1.49/log10 Paul Ehrlich Institute units/mL [1.08-2.07], respectively). Cutoffs with the highest accuracy in predicting HBeAg seroclearance at 36 months were qHBcrAg <6.5 log10 U/mL at month 24 (Se, 1; Sp, 0.58) and baseline qAnti-HBc ≥4.1 log10 Paul Ehrlich Institute units/mL (Se, 0.42; Sp, 0.81).Conclusions: In coinfected patients undergoing TDF, qHBcrAg/qAnti-HBc could be of use in monitoring HBeAg seroclearance
    corecore