Short-term treatment outcomes in human immunodeficiency virus type-1 and hepatitis B virus co-infections.

BACKGROUND: Co-infection of HIV with HBV is common in West Africa but little information is available on the effects of HBV on short-term therapy for HIV patients. A 28 day longitudinal study was conducted to examine short-term antiretroviral therapy (ART) outcomes in HIV infected individuals with HBV co-infection. METHODS: Plasma from 18 HIV infected individuals co-infected with HBV and matched controls with only HIV infection were obtained at initiation, and 7 and 28 days after ART. HIV-1 viral load changes were monitored. Clinical and demographic data were also obtained from patient folders, and HIV-1 drug resistance mutation and subtype analysis performed. RESULTS: The presence of HBV co-infection did not significantly affect HIV-1 viral load changes within 7 or 28 days. The CD4(+) counts on the other hand of patients significantly affected the magnitude of HIV-1 viral load decline after 7 days (ρ = -0.441, p = 0.040), while the pre-ART HIV-1 VL (ρ = 0.844, p = <0.001) and sex (U = 19.0, p = 0.020) also determined HIV-1 viral load outcomes after 28 days of ART. Even though the geometric sensitivity score of HIV-1 strains were influenced by the HIV-1 subtypes (U = 56.00; p = 0.036), it was not a confounder for ART outcomes. CONCLUSIONS: There may be the need to consider the confounder effects of sex, pre-ART CD4(+), and pre-ART HIV-1 viral load in the discourse on HIV and HBV co-infection.

Prevalence and impact of hepatitis B and C virus co-infections in antiretroviral treatment naïve patients with HIV infection at a major treatment center in Ghana.

Data on the effects of the presence of hepatitis B virus (HBV) and hepatitis C virus (HCV) in patients co-infected with these viruses and HIV in West Africa are conflicting and little information is available in Ghana. A cohort of 138 treatment naïve individuals infected with HIV was screened for HBV and HCV serologic markers; HBsAg positive patients were tested for HBeAg, anti-HBe, and anti-HBc IgM. The viral load of HIV-1 in the plasma was determined in 81 patients. Eighteen of the 138 patients (13%) and 5 (3.6%) had HBsAg and anti-HCV, respectively. None of the patients had anti-HBc IgM, but 10 (55.6%) and 8 (44.4%) of the 18 patients who were HBsAg positive had HBeAg and anti-HBe, respectively. In patients with measurement of CD4(+) undertaken within 1 month (n = 83), CD4(+) count was significantly lower in patients with HBeAg (median [IQR], 81 [22-144]) as compared to those with anti-HBe (median [IQR], 210 [197-222]) (P = 0.002, CI: -96.46 to 51.21). However, those with HIV mono-infection had similar CD4(+) counts (median [IQR], 57 [14-159]) compared to those with HBeAg (P = 1.0, CI: -71.75 to 73.66). Similar results were obtained if CD4(+) count was measured within 2 months prior to initiation of HAART (n = 119). Generally, HBV and anti-HCV did not affect CD4(+) and viral loads of HIV-1 in plasma but patients with HIV and HBV co-infection who had HBeAg had more severe immune suppression as compared to those with anti-HBe. This may have implication for initiating HAART in HBV endemic areas.

Variability of the human immunodeficiency virus type 1 polymerase gene from treatment naïve patients in Accra, Ghana.

BACKGROUND: Little is known about the HIV-1 drug resistance mutations in Ghana. OBJECTIVES: To determine the background protease (PR) and reverse transcriptase (RT) mutations of HIV-1 from treatment naïve patients in Ghana. STUDY DESIGN: Twenty-five plasma samples randomly selected were analyzed for drug resistance mutations. The molecular phylogeny and recombinant patterns of the polymerase gene of HIV-1 were also analysed. RESULTS: No major drug-resistance mutations were seen in protease or reverse transcriptase genes. The L10I, L10V, V11I and E35G minor mutations were seen in four patients, while the V179E was observed in a patient with subtype G. An insertion of lysine was found at codon 36 of the protease gene of one patient. The predominant subtype was the CRF02_AG strain (n=22), but 3 (13.6%) of these were recombinants with HIV-1 subtype K and/or A1. Two patients harboured unclassified/complex strains with D/CRF01_AE and G/CRFAG_02 subtypes for the PR and RT, respectively, using the Stanford Database. Viral loads (VL) ranged from 2290 to >1,500,000c/ml (mean=339,065c/ml). CONCLUSIONS: Treatment naïve patients in Ghana before scale-up may have minor but not major PR mutations and high viral loads. The clinical effects of minor mutations/polymorphisms in the PR and RT genes and recombinants need to be investigated.