Hepatitis B virus coinfection negatively impacts HIV outcomes in HIV seroconverters

Helen M. Chun, Mollie P. Roediger, Katherine Huppler Hullsiek, Chloe L. Thio, Brian K. Agan, William P. Bradley, Sheila A. Peel, Linda L. Jagodzinski, Amy C. Weintrob, Anuradha Ganesan, Glenn Wortmann, Nancy F. Crum-Cianflone, Jason D. Maguire, Michael L. Landrum

Research output: Contribution to journalArticlepeer-review

80 Scopus citations

Abstract

Background. Understanding the impact of hepatitis B virus (HBV) in human immunodeficiency virus (HIV) coinfection has been limited by heterogeneity of HIV disease. We evaluated HBV coinfection and HIV-related disease progression in a cohort of HIV seroconverters. Methods. Participants with HIV diagnosis seroconversion window of ≤3 years and serologically confirmed HBV infection (HB) status were classified at baseline into 4 HB groups. The risk of clinical AIDS/death in HIV seroconverters was calculated by HB status. Results. Of 2352 HIV seroconverters, 474 (20%) had resolved HB, 82 (3%) had isolated total antibody to hepatitis B core antigen (HBcAb), and 64 (3%) had chronic HB. Unadjusted rates (95% confidence intervals [CIs]) of clinical AIDS/death for the HB-negative, resolved HB, isolated HBcAb, and chronic HB groups were 2.43 (2.15-2.71); 3.27 (2.71-3.84); 3.75 (2.25-5.25); and 5.41 (3.41-7.42), respectively. The multivariable risk of clinical AIDS/death was significantly higher in the chronic HB group compared to the HB-negative group (hazard ratio [HR], 1.80; 95% CI, 1.20-2.69); while the HRs were increased but nonsignificant for those with resolved HB (HR, 1.17; 95% CI,. 94-1.46) and isolated HBcAb (HR, 1.14; 95% CI,. 75-1.75). Conclusions. HBV coinfection has a significant impact on HIV outcomes. The hazard for an AIDS or death event is almost double for those with chronic HB compared, with HIV-monoinfected persons.

Original languageEnglish (US)
Pages (from-to)185-193
Number of pages9
JournalJournal of Infectious Diseases
Volume205
Issue number2
DOIs
StatePublished - Jan 15 2012

Bibliographical note

Funding Information:
Financial support. This work was supported by the Infectious Disease Clinical Research Program (IDCRP; www.idcrp.org), a Department of Defense program executed through Uniformed Services University of the Health Sciences. This project has been funded in whole, or in part, with federal funds from the National Institute of Allergy and Infectious Diseases, National Institutes of Health (NIH), under Inter-Agency Agreement Y1-AI-5072. The IDCRP reviewed the study design, collected the data and provided salary support to investigators (M. L. L., K. H. H., M. P. R., N. F. C., A. C. W., A. G., and B. K. A.). The analyses, conclusions, and decision to submit the manuscript are the independent work and decision of the authors.

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