TY - JOUR
T1 - Mortality in relation to hepatitis B virus (HBV) infection status among HIV-HBV co-infected patients in sub-Saharan Africa after immediate initiation of antiretroviral therapy
AU - Mohareb, Amir M.
AU - Kouamé, Gérard Menan
AU - Gabassi, Audrey
AU - Gabillard, Delphine
AU - Moh, Raoul
AU - Badje, Anani
AU - Emième, Arlette
AU - Maylin, Sarah
AU - Ménan, Hervé
AU - Hyle, Emily P.
AU - Delaugerre, Constance
AU - Danel, Christine
AU - Anglaret, Xavier
AU - Lacombe, Karine
AU - Eholié, Serge P.
AU - Boyd, Anders
N1 - Funding Information: This work was supported by the Agence Nationale de Rercheches sur le SIDA et les hépatites virales (ANRS) and SIDACTION, Paris, France. GMK also received doctoral funding from the ANRS. AMM received funding from National Institutes of Health NIAID T32AI007433 and NIAID R37AI058736. EPH received funding from National Institutes of Health NHLBI K01HL123349. Its contents are solely the responsibility of the authors and do not necessarily represent the official views of the NIH. Funding Information: This work was supported by the Agence Nationale de Rercheches sur le SIDA et les h?patites virales (ANRS) and SIDACTION, Paris, France. GMK also received doctoral funding from the ANRS. AMM received funding from National Institutes of Health NIAID T32AI007433 and NIAID R37AI058736. EPH received funding from National Institutes of Health NHLBI K01HL123349. Its contents are solely the responsibility of the authors and do not necessarily represent the official views of the NIH. We thank all patients who participated in this trial; members of SMIT, CeDReS, CEPREF, USAC, CIRBA, CNTS, La Pierre Angulaire, Hopital General Abobo, Formation Sanitaire Anonkoua Koute, Centre de sante El Rapha, the Programme PACCI team, and INSERM U1219 IDLIC teams for their valuable contributions; Gilead Sciences, for the donation of Truvada; and Merck Sharp & Dohme, for the donation of Stocrin. Publisher Copyright: © 2020 John Wiley & Sons Ltd
PY - 2021/4
Y1 - 2021/4
N2 - It is unknown how past and active hepatitis B virus (HBV) infection affect immunorecovery and mortality in people with HIV who initiate tenofovir-based antiretroviral therapy (ART). Using data collected between 2008 and 2015, we studied people with HIV in sub-Saharan Africa initiating immediate ART in the Temprano randomized control trial. We classified participants into HBV groups at ART initiation: hepatitis B surface antigen (HBsAg)-positive with HBV DNA ≥ 2,000 IU/ml; HBsAg-positive with HBV DNA < 2,000 IU/ml; isolated HBcAb-positive; resolved infection (HBsAb-positive/HBcAb-positive); and HBV non-immune/vaccinated (HBcAb-negative). We compared square-root CD4-cell count increases using mixed-effect, non-linear regression adjusted for age, sex, baseline CD4 cell count, and HIV RNA. We compared all-cause mortality using Bayesian parametric survival regression. Among 879 participants, 24 (2.7%) had HBsAg with high HBV DNA, 76 (8.6%) HBsAg with low HBV DNA, 325 (37.0%) isolated anti-HBcAb, 226 (25.7%) resolved HBV infection and 228 (25.9%) HBV non-immune/vaccinated. We found no significant difference in CD4 cell increases between HBV-infection groups after adjustment (p = 0.16). Participants with HBsAg and high HBV DNA had the highest incidence of all-cause mortality (1.9/100 person-years, 95% Credibile Interval [CrI] = 1.0–3.4). By comparison, incidence rates of mortality were reduced by 57% (95%CrI = −79%, −13%), 60% (95%CrI = −82%, −12%) and 66% (95%CrI = −84%, −23%) in those who had isolated anti-HBcAb-positive, resolved HBV infection and HBV non-immune/vaccinated, respectively. In conclusion, individuals with HIV and past HBV infection or isolated anti-HBcAb-positive serology, much like HBV non-immune/vaccinated, experience lower mortality than those with HBsAg and high HBV DNA. Additional HBV-related management would not be necessary for these individuals.
AB - It is unknown how past and active hepatitis B virus (HBV) infection affect immunorecovery and mortality in people with HIV who initiate tenofovir-based antiretroviral therapy (ART). Using data collected between 2008 and 2015, we studied people with HIV in sub-Saharan Africa initiating immediate ART in the Temprano randomized control trial. We classified participants into HBV groups at ART initiation: hepatitis B surface antigen (HBsAg)-positive with HBV DNA ≥ 2,000 IU/ml; HBsAg-positive with HBV DNA < 2,000 IU/ml; isolated HBcAb-positive; resolved infection (HBsAb-positive/HBcAb-positive); and HBV non-immune/vaccinated (HBcAb-negative). We compared square-root CD4-cell count increases using mixed-effect, non-linear regression adjusted for age, sex, baseline CD4 cell count, and HIV RNA. We compared all-cause mortality using Bayesian parametric survival regression. Among 879 participants, 24 (2.7%) had HBsAg with high HBV DNA, 76 (8.6%) HBsAg with low HBV DNA, 325 (37.0%) isolated anti-HBcAb, 226 (25.7%) resolved HBV infection and 228 (25.9%) HBV non-immune/vaccinated. We found no significant difference in CD4 cell increases between HBV-infection groups after adjustment (p = 0.16). Participants with HBsAg and high HBV DNA had the highest incidence of all-cause mortality (1.9/100 person-years, 95% Credibile Interval [CrI] = 1.0–3.4). By comparison, incidence rates of mortality were reduced by 57% (95%CrI = −79%, −13%), 60% (95%CrI = −82%, −12%) and 66% (95%CrI = −84%, −23%) in those who had isolated anti-HBcAb-positive, resolved HBV infection and HBV non-immune/vaccinated, respectively. In conclusion, individuals with HIV and past HBV infection or isolated anti-HBcAb-positive serology, much like HBV non-immune/vaccinated, experience lower mortality than those with HBsAg and high HBV DNA. Additional HBV-related management would not be necessary for these individuals.
KW - CD4+ cell count
KW - HIV
KW - hepatitis B virus
KW - mortality
KW - sub-Saharan Africa
UR - http://www.scopus.com/inward/record.url?scp=85099841459&partnerID=8YFLogxK
U2 - https://doi.org/10.1111/jvh.13461
DO - https://doi.org/10.1111/jvh.13461
M3 - Article
C2 - 33382189
SN - 1352-0504
VL - 28
SP - 621
EP - 629
JO - Journal of viral hepatitis
JF - Journal of viral hepatitis
IS - 4
ER -