Background As HAART is introduced into areas of the world with high hepatitis B virus (HBV) endemicity, it is important to determine the influence of HBV on HIV-HBV co-infected persons receiving antiretroviral therapy (ART). Methods We studied 1,564 HIV-infected subjects in Jos, Nigeria who initiated ART. HIV-HBV co-infected participants had HBeAg and HBV DNA status determined. CD4+ T-cell count and HIV viral load at ART initiation were compared between HIV mono-infected and HIV-HBV co-infected subjects using univariate methods. Regression analyses were used to determine if HBeAg status or HBV DNA at ART initiation were associated with baseline HIV parameters or ART response. Results The CD4+ T-cell counts of the 262 (16.7%) HIV-HBV co-infected participants was 107 cells/mL compared to 130 cells/mL in HIV monoinfected participants (p <0.001) at ART initiation. HIV-HBV co-infected participants also had higher HIV viral loads than HIV monoinfected subjects (4.96 vs. 4.75 log10 copies/mL; p = 0.02). Higher HBV DNA and detectable HBeAg were independently associated with lower CD4+ T-cell counts at ART initiation but not with higher HIV viral load. In a multivariable model, HBeAg-positive subjects were less likely to suppress HIV replication to ≤400 copies/ml (OR 0.54, p=0.03) at 24 weeks, but they had similar CD4+ T cell increases. At 48 weeks, there was no significant effect of HBeAg status on ART response. Conclusions In HIV-infected Nigerian individuals, HBV co-infection, especially in those with high levels of HBV replication, was associated with lower CD4+ T-cell counts at ART initiation independent of HIV RNA level. Subjects with HBeAg positive status had a slower virological response to ART. Further work is needed to understand the effects of HBV on CD4+ T-cells.

The effect of HCV on ART response in patients in sub-Saharan Africa is unknown. We studied 1431 HIV-infected ART initiators in Jos, Nigeria of whom 6% were HCV co-infected. A similar proportion of HIV-HCV co-infected and HIV-mono-infected patients achieved HIV RNA <400 cp/ml after 24 and 48 weeks of ART (p values >0.05). Hepatotoxicity was uncommon (0.8% and 0.33% at 24 and 48 weeks, respectively), but was more common in the HIV-HCV co-infected group at 24 (aOR=19.3; 95% CI: 4.41–84.4) and 48 weeks (aOR=56.7; 95% CI: 5.03–636.92). HCV did not significantly impact ART response in this Nigerian cohort.