Publications (3)13.58 Total impact
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ABSTRACT: 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.JAIDS Journal of Acquired Immune Deficiency Syndromes 11/2012; · 4.43 Impact Factor
Article: Impact of hepatitis B virus infection on human immunodeficiency virus response to antiretroviral therapy in Nigeria.[show abstract] [hide abstract]
ABSTRACT: As highly active antiretroviral therapy (ART) is introduced into areas of the world in which hepatitis B virus (HBV) infection is highly endemic, it is important to determine the influence of HBV on persons with human immunodeficiency virus (HIV) and HBV coinfection who are receiving ART. We studied 1564 HIV-infected patients in Jos, Nigeria, who initiated ART. Participants with HIV-HBV coinfection had hepatitis B e antigen (HBeAg) and HBV DNA status determined. CD4+ T cell count and HIV load at ART initiation were compared between individuals with HIV monoinfection and those with HIV-HBV coinfection with use of 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. The median CD4+ T cell count of the 262 participants with HIV-HBV coinfection (16.7%) was 107 cells/mL, compared with 130 cells/mL for participants with HIV monoinfection at ART initiation (P = .001). Participants with HIV-HBV coinfection also had higher HIV loads than did patients with HIV monoinfection (4.96 vs 4.75 log10 copies/mL; p = .02 ). Higher HBV DNA and detectable HBeAg levels were independently associated with lower CD4+ T cell counts at ART initiation but not with higher HIV loads. In a multivariable model, HBeAg-positive patients were less likely than HBeAg-negative patients to suppress HIV replication to <or= 400 copies/mL (odds ratio, 0.54; P = .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. Among HIV-infected Nigerian individuals, HBV coinfection, especially among those with high levels of HBV replication, was associated with lower CD4+ T cell counts at ART initiation, independent of HIV RNA level. Patients with HBeAg-positive status had a slower virological response to ART, compared with HBeAg-negative patients. Further work is needed to understand the effects of HBV on CD4+ T cells.Clinical Infectious Diseases 10/2009; 49(8):1268-73. · 9.15 Impact Factor
Article: Effect of HBV DNA Levels on HIV Infection and Response to ART in a HIV/HBV Co-infected Nigerian Cohort[show abstract] [hide abstract]
ABSTRACT: Background: In a Nigerian HIV-HBV co-infected cohort, we showed that hepatitis B was associated with lower CD4 counts and higher HIV RNA prior to antiretroviral therapy (ART). We hypothesized that high HBV DNA levels would influence pre-ART HIV stage and ART-related hepatotoxicity, but that it would not affect ART response. Methods: We tested our hypothesis in HIV+/HCV-patients who initiated ART through PEPFAR in Nigeria. We compared HIV parameters between a control group of HIV+/HBV-/HCV-(HIV only) patients and several HIV/HBV coinfected (HBsAg+) groups stratified according to HBV DNA levels (≥20,000 IU/ml) and HBeAg status. Comparisons were made at baseline and after months 3 and 6 of ART using nonparametric tests for continuous variables and Fisher's exact tests for categorical variables. Hepatotoxicity was defined according to ACTG definitions. Results: There were 1,305 HIV only and 264 HIV/HBV patients, of which 263 (99.6%) and 226 (86%) were tested for HBeAg and HBV DNA, respectively. Median baseline CD4 count (cells/mm3) was lower in the HIV/HBV group with high HBV DNA (89) compared to the HIV only or the HIV/HBV with low HBV DNA (130 and 129, respectively; p=0.001). Stratification by HBeAg revealed that the median baseline CD4 count in the HBeAg-, low HBV DNA was similar to the HIV only group (129 and 130 cells, respectively); all other groups had lower median baseline counts. The median baseline HIV RNA was similar between the HIV/HBV groups with high and low HBV DNA (89,882 and 96,895 c/ml), which was significantly higher than the HIV only group (55,708 c/ml; p=0.01). After 6 months of ART, neither HBV DNA nor HBeAg status altered the percent with HIV RNA <400 c/ml. CD4 counts increased in all groups at 6 months, but those with high HBV DNA had lower median CD4 counts (216 vs 229 for low HBV DNA and 240 for HIV only, p=0.08). HBeAg status did not alter this relationship. The high HBV DNA group had significantly higher median baseline ALT (p=0.0002) and the greatest cumulative hepatotoxicity by month 6 (12.1% vs. 3.9-4.9%, P=0.01). Conclusions: In this HIV/HBV co-infected Nigerian cohort, high HBV DNA levels were associated with lower baseline CD4 counts and increased risk for hepatotoxicity on ART. High HBV DNA levels did not clearly impair immunological and virological responses with 6 months of ART, but CD4 counts remained lower in those with high HBV DNA. Further studies are needed to understand the impact of HBV on HIV therapy and management.