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. 2016 Aug 16;3(3):ofw140.
doi: 10.1093/ofid/ofw140. eCollection 2016 Sep.

Slow CD4+ T-Cell Recovery in Human Immunodeficiency Virus/Hepatitis B Virus-Coinfected Patients Initiating Truvada-Based Combination Antiretroviral Therapy in Botswana

Affiliations

Slow CD4+ T-Cell Recovery in Human Immunodeficiency Virus/Hepatitis B Virus-Coinfected Patients Initiating Truvada-Based Combination Antiretroviral Therapy in Botswana

Motswedi Anderson et al. Open Forum Infect Dis. .

Abstract

Background. Hepatitis B virus (HBV) and human immunodeficiency virus (HIV) coinfection has emerged as an important cause of morbidity and mortality. We determined the response to Truvada-based first-line combination antiretroviral therapy (cART) in HIV/HBV-coinfected verus HIV-monoinfected patients in Botswana. Methods. Hepatitis B virus surface antigen (HBsAg), HBV e antigen (HBeAg), and HBV deoxyribonucleic acid (DNA) load were determined from baseline and follow-up visits in a longitudinal cART cohort of Truvada-based regimen. We assessed predictors of HBV serostatus and viral suppression (undetectable HBV DNA) using logistic regression techniques. Results. Of 300 participants, 28 were HBsAg positive, giving an HIV/HBV prevalence of 9.3% (95% confidence interval [CI], 6.3-13.2), and 5 of these, 17.9% (95% CI, 6.1-36.9), were HBeAg positive. There was a reduced CD4+ T-cell gain in HIV/HBV-coinfected compared with HIV-monoinfected patients. Hepatitis B virus surface antigen and HBeAg loss was 38% and 60%, respectively, at 24 months post-cART initiation. The HBV DNA suppression rates increased with time on cART from 54% to 75% in 6 and 24 months, respectively. Conclusions. Human immunodeficiency virus/HBV coinfection negatively affected immunologic recovery compared with HIV-1C monoinfection. Hepatitis B virus screening before cART initiation could help improve HBV/HIV treatment outcomes and help determine treatment options when there is a need to switch regimens.

Keywords: Botswana; HIV/HBV coinfection; Truvada; hepatitis B virus; tenofovir.

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Figures

Figure 1.
Figure 1.
Kaplan–Meier curve for proportion of hepatitis B virus surface antigen (HBsAg) loss from baseline to 24 months.
Figure 2.
Figure 2.
Kaplan–Meier curve for proportion of hepatitis B virus (HBV) deoxyribonucleic acid (DNA) loss from baseline to 24 months.
Figure 3.
Figure 3.
Maximum likelihood tree showing Botswana hepatitis B virus (HBV) fragment (415- base pair) and GenBank HBV references. Study isolates are marked by their accession and colored shapes (green for genotype A and red for genotype D), whereas the reference strains are represented by their subgenotypes, accession numbers, followed by their country of origin, as they appear in GenBank.
Figure 4.
Figure 4.
Comparison of hepatitis B virus (HBV) viral load proportions between HBV genotypes A and D after 24 months from enrollment.
Figure 5.
Figure 5.
Comparison of CD4+ T-cell count change from baseline by hepatitis B virus (HBV) status to 24 months. Abbreviation: HIV, human immunodeficiency virus.
Figure 6.
Figure 6.
Comparison of CD4+ T-cell count change from baseline by sex.

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