An evaluation of the diagnostic performance characteristics of the Yellow Fever IgM immunochromatographic rapid diagnostic test kit from SD Biosensor in Ghana.

Yellow fever is endemic in Ghana and outbreaks occur periodically. The prodromal signs due to Yellow Fever Virus (YFV) infection are non-specific, making clinical signs unreliable as the sole criteria for diagnosis. Accurate laboratory confirmation of suspected yellow fever cases is therefore vital in surveillance programs. Reporting of ELISA IgM testing results by laboratories can delay due to late arrival of samples from the collection sites as well as limited availability of ELISA kits. In this study, the diagnostic performance characteristics of a rapid immunochromatographic Standard Q Yellow Fever IgM test kit (SD Biosensor) was evaluated for the rapid diagnosis of Yellow Fever infection in Ghana. A panel of 275 sera, comprising 81 confirmed YFV positives and 194 negatives were re-tested in this study using the Standard Q Yellow Fever IgM test kit. Using the CDC/WHO Yellow Fever IgM capture ELISA as a benchmark, the sensitivity, specificity and accuracy of the Standard Q Yellow Fever test kit were 96.3%, 97.9% and 97.5%, respectively. The false positivity rate was 5.1% and there was no cross-reactivity when the Standard Q Yellow Fever test kit was tested against dengue, malaria and hepatitis B and C positive samples. In addition, inter-reader variability and invalid rate were both zero. The results indicate that the diagnostic performance of the Standard Q Yellow Fever IgM test kit on serum or plasma is comparable to the serum IgM detection by ELISA and can be used as a point of care rapid diagnostic test kit for YFV infection in endemic areas.

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.