Hepatitis B surface antigen loss in individuals with... : AIDS (original) (raw)

BASIC SCIENCE

Hepatitis B surface antigen loss in individuals with chronic hepatitis B virus and HIV-1 infections in Botswana

Mpebe, Gorata G.A.a,b; Phinius, Bonolo B.a,c; Mutenga, Sharona,d; Baruti, Kaboa,b; Bhebhe, Lynnettea; Choga, Wonderful T.a,c; Jongman, Mosimanegapea,b; Pretorius-Holme, Mollye; Gaolathe, Tendania; Mmalane, Mompatia,e; Shapiro, Rogera,e; Makhema, Josepha,e; Lockman, Shahina,e; Moyo, Sikhulilea,c,e,f; Anderson, Motswedia; Gaseitsiwe, Simania,e

aBotswana Harvard AIDS Institute Partnership

bBiological Sciences, Faculty of Science

cSchool of Allied Health Professions, Faculty of Health Sciences, University of Botswana, Gaborone, Botswana

dMidlands State University, Gweru, Zimbabwe

eDepartment of Immunology and Infectious Diseases, Harvard T.H. Chan School of Public Health, Boston, Massachusetts, USA

fSchool of Health Systems and Public Health, University of Pretoria, Gauteng, South Africa.

Correspondence to Simani Gaseitsiwe, PhD, Botswana Harvard Botswana Harvard AIDS Institute Partnership, Private Bag BO 320, Gaborone, Botswana. Tel: +267 3902671; fax: +267 390 1284; e-mail: [email protected]

Received 13 June, 2023

Revised 5 September, 2023

Accepted 21 September, 2023

Abstract

Objectives:

We sought to determine hepatitis B surface antigen (HBsAg) loss and its predictors among people with chronic hepatitis B (CHB) infections and HIV (PWH) in Botswana.

Methods:

Archived plasma samples from a cohort of PWH in Botswana (2013–2018) with 3 yearly time-points were used. Samples were screened for HBsAg, immunoglobulin M HBV core antibodies (anti-HBc IgM) and HBV e-antigen (HBeAg) at all time points. HBV deoxyribonucleic acid (DNA) quantification was done at baseline. The Wilcoxon rank-sum was used to compare continuous variables while the chi-squared test and Fishers exact test were used for categorical data wherever appropriate. Logistic regression was used to assess predictors of seroclearance.

Results:

Of 141 participants with HBsAg-positive serology (HBsAg+) at baseline, 92.2% (131/141) [95% confidence interval (CI) 87.4–96.1] were persistently HBsAg+ at year 1. We report a HBsAg loss of 7.1% (10/141) (95% CI 3.9–12.6) among participants with negative HBeAg and negative IgM serologies. HBsAg loss was 6.3% (7/111) among antiretroviral therapy (ART)-experienced participants and 10.7% (3/28) (95% CI 0.4–5.0) in ART-naive participants. Most participants who had positive anti-HBc IgM serology and did not lose HBsAg were on either lamivudine (3TC)-based therapy or non-tenofovir disoproxil fumarate (TDF)-based therapy, except for one participant. The participants also had varying HBeAg status. HBsAg loss was independent of HIV viral load, CD4+ cell count, age, and sex.

Conclusion:

We report a HBsAg loss of 6.3% over a 3-year period among ART-experienced CHB participants. Future studies that focus on HBsAg loss in mono-infected patients and the possible correlation between HBeAg status and HBsAg loss are warranted.