CD4+ T Cell Recovery and Hepatitis B Virus Coinfection in HIV-Infected Patients from Côte d'Ivoire Initiating Antiretroviral Therapy

Laura Houghtaling, Raoul Moh, Mariama Abdou Chekaraou, Delphine Gabillard, Xavier Anglaret, Serge Paul Eholié, Fabien Zoulim, Christine Danel, Karine Lacombe, Anders Boyd

Research output: Contribution to journalArticlepeer-review

4 Scopus citations

Abstract

Immunorecovery could be attenuated in HIV-hepatitis B virus (HBV) coinfection versus HIV monoinfection during antiretroviral therapy (ART), yet, whether it also occurs in individuals from sub-Saharan Africa without severe comorbidities is unknown. In this study, 808 HIV-infected patients in Côte d'Ivoire initiating continuous ART were included. Six-month CD4+ count trajectories and the proportion reaching CD4+ T cell counts >350/mm 3 , HIV-RNA <300 copies/mL, still alive and not lost to follow-up within 18 months ("optimal immunorecovery") were compared between coinfected groups. At inclusion, 80 (9.9%) patients were HIV-HBV coinfected, 40 (50.0%) of whom had high HBV-DNA viral load (VL) (>10 4 copies/mL). Coinfected patients with high HBV-DNA replication initiated ART with significantly lower median CD4+ T cell counts [216/mm 3 , interquartile range (IQR) = 150-286] compared to coinfection with low HBV-DNA replication (268/mm 3 , IQR = 178-375) or HIV monoinfection (257/mm 3 , IQR = 194-329) (p = .003). These patients had significantly faster rates of CD4+ cell count increase from baseline after adjusting for baseline age, World Health Organization stage III/IV, and CD4+ cell counts (p = .04), yet, were not more likely to exhibit optimal immunorecovery (82.5% vs. 80.0% and 77.9%, respectively) (p = .8). In conclusion, change in CD4+ cell counts after ART-initiation was accelerated in coinfected patients with high HBV DNA VLs, but this did not lead to increased rates of optimal immunorecovery.

Original languageEnglish (US)
Pages (from-to)439-445
Number of pages7
JournalAIDS Research and Human Retroviruses
Volume34
Issue number5
DOIs
StatePublished - May 2018

Bibliographical note

Funding Information:
We thank all patients who participated in the Trivacan trial. We also gratefully acknowledge the valuable contributions of the SMIT, CeDReS, CEPREF, USAC, CIRBA, CNTS, the Programme PACCI team, as well as INSERM exU593 and U897 teams. This work was supported by funds from the Agence Nationale de Recherche sur le Sida et les Hépatites (ANRS 1269/ANRS 12104 and ANRS 12240). A postdoctoral fellowship from the ANRS and SIDACTION was awarded to A.B. for some of the work presented in this article.

Publisher Copyright:
© Copyright 2018, Mary Ann Liebert, Inc. 2018.

Keywords

  • antiretroviral therapy
  • immune restoration
  • sub-Saharan Africa
  • treatment response
  • viral replication

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