Serge Théophile Soubeiga

APOBEC3G Variants and Protection against HIV-1 Infection in Burkina Faso

Studies on host factors, particularly the APOBEC3G gene, have previously found an association with AIDS progression in some populations and against some HIV-1 strains but not others. Our study had two main objectives: firstly, to screen a population from Burkina Faso for three variants of APOBEC3G previously described, and secondly to analyze the effect of these three variants and their haplotypes on HIV-1 infection with Circulating Recombinant Forms (CRFs) present in Burkina Faso. This case control study involved 708 seropositive and seronegative individuals. Genotyping was done by the TaqMan allelic discrimination method. Minor allele frequencies of rs6001417 (p<0.05), rs8177832 (P<0.05), and rs35228531 (P<0.001) were higher in seronegative subjects. The rs6001417 and rs8177832 SNPs were associated with HIV-1 infection in an additive model (P<0.01). Furthermore the SNP rs35228531 was also associated with HIV-1 infection in a dominant model (P<0.001). Odds ratio analysis of genotypes and alleles of the different APOBEC3G variants showed that there is a strong association between the minor genetic variants, genotype of the three SNPs, and HIV-1 status. Haplotype analysis demonstrated that rs6001417, rs8177832, and rs35228531 are in linkage disequilibrium. The haplotype GGT from the rs6001417, rs8177832 and rs35228531 respectively has a protective effect OR = 0.54 [0.43–0.68] with P<0.001. There was also associations between the haplotypes GGC OR = 1.6 [1.1;-2.3] P<0.05, and CGC OR = 5.21 [2.4–11.3] P<0.001, which increase the risk of infection by HIV-1 from almost two (2) to five (5) fold. This study demonstrates an association of rs6001417, rs8177832, and rs35228531 of APOBEC3G with HIV-1 infection in a population from Burkina Faso.

Effectiveness of the prevention of mother-to-child transmission of HIV protocol applied at Saint Camille Medical Centre in Ouagadougou, Burkina Faso.

Despite many prevention efforts, the number of children infected by HIV in sub‐Saharan Africa through vertical transmission remains high. This infection can be reduced through programmes of prevention of mother‐to‐child HIV transmission (PMTCT). The objective of this study was to evaluate the effectiveness of the PMTCT protocol at Saint Camille Medical Centre in Ouagadougou, Burkina Faso.

Human immunodeficiency virus type 1 drug resistance in a subset of mothers and their infants receiving antiretroviral treatment in Ouagadougou, Burkina Faso

The emergence of HIV-1 drug resistance (HIVDR) is a public health problem that affects women and children. Local data of HIVDR is critical to improving their care and treatment. So, we investigated HIVDR in mothers and infants receiving antiretroviral therapy (ART) at Saint Camille Hospital of Ouagadougou, Burkina Faso. This study included 50 mothers and 50 infants on ART. CD4 and HIV-1 viral load were determined using FACSCount and Abbott m2000rt respectively. HIVDR was determined in patients with virologic failure using ViroSeq HIV-1 Genotyping System kit on the 3130 Genetic Analyzer. The median age was 37.28 years in mothers and 1.58 year in infants. Sequencing of samples showed subtypes CRF02_AG (55.56%), CRF06_cpx (33.33%) and G (11.11%). M184V was the most frequent and was associated with highlevel resistance to 3TC, FTC, and ABC. Other mutations such as T215F/Y, D67N/E, K70R, and K219Q were associated with intermediate resistance to TDF, AZT, and 3TC. No mutation to LPV/r was detected among mothers and infants. The findings of HIVDR in some mothers and infants suggested the change of treatment for these persons.

Prevalence, genetic variants and clinical implications of G-6-PD deficiency in Burkina Faso: a systematic review

BackgroundIt is now well-known that some antimalarials such as primaquine may induce severe hemolytic anemia in people with G-6-PD deficiency. Antimalarial drug prescriptions must, therefore take into account the patient’s G-6-PD status in malaria endemic areas such as Burkina Faso, where the prevalence of this genetic abnormality is relatively high. Although great clinical heterogeneity is observed depending on the molecular nature of the deficiency and the residual enzyme activity in the red blood cell, there is very poor data on the prevalence of G-6-PD deficiency and the distribution of involved genetic variants in Burkina Faso. In this systematic review, we present a synthesis of the various studies carried out on the G-6-PD deficiency in Burkina Faso in order to determine its prevalence, probable distribution of the genetic variants involved and their clinical implications for a national systematic screening policy among the groups most vulnerable to malaria.MethodsA systematic review was carried out to analyze available published data on the prevalence, phenotypes and mutations responsible for G-6-PD deficiency in Burkina Faso. The key words used were “G-6-PD deficiency AND Burkina Faso” or “Déficit en G-6-PD AND Burkina Faso” in French. To identify the relevant articles, two independent reviewers reviewed the titles, abstracts and the full text of the selected papers.ResultsAn average prevalence of 16.6% (183/1100; CI 95%: 0.145–0.190) and 6.5% (69/1066; CI 95%: 0.051–0.081) of G-6-PD deficiency was found respectively in men and women in this systematic review. Although the predominance (99.8% of G-6-PD deficient cases) of 202A/376G G-6-PD A- variant, the Santamaria and Betica Selma variants were identified in Burkina Faso. Independently of the method used, the enzymatic deficiency was significantly higher in males (2.5–20.5%) compared to females (3.3–12.3%).ConclusionThis systematic review suggests that despite the ubiquity of the 202A/376G G-6-PD A- variant in Burkina Faso, it will be necessary to consider the Santamaria and Betica Selma variants although their frequencies remain to be specified. A systematic screening of the G-6-PD deficiency is also needed to prevent the occurrence of iatrogenic hemolytic accidents.RésuméContexteIl est. actuellement bien connu que certains antipaludiques comme la primaquine, peuvent induire des crises d’anémie hémolytique graves chez les personnes présentant un déficit en G-6-PD. Les prescriptions de médicaments antipaludiques doivent donc tenir compte du statut G-6-PD du patient dans les zones d’endémie du paludisme comme le Burkina Faso où la prévalence de cette anomalie génétique est. relativement élevée. En dépit d’une grande hétérogénéité clinique observée selon la nature moléculaire du déficit et l’activité résiduelle de l’enzyme dans le globule rouge, il existe très peu de données sur la prévalence du déficit en G-6-PD et la distribution des variants génétiques en cause au Burkina Faso. Dans cette revue de la littérature nous présenterons la synthèse des différents travaux réalisés sur le déficit en G-6-PD au Burkina Faso afin de déterminer sa prévalence, la distribution probable des variants génétiques en cause et leurs implications cliniques en vue d’une politique nationale de dépistage systématique au sein des groupes les plus vulnérables au paludisme.MéthodesUne revue systématique a été réalisée pour analyser les données publiées disponibles sur la prévalence, les phénotypes et les mutations du déficit en G-6-PD au Burkina Faso Les mots clés utilisés étaient « G6PD deficiency AND Burkina Faso » en anglais ou « Déficit en G6PD AND Burkina Faso en français ». Pour identifier les articles pertinents, deux examinateurs indépendants ont examiné les titres, les résumés et le texte intégral des articles retenus.RésultatsUne prévalence moyenne de 16,6% (183/1100; IC 95%: 0,145–0,190) et 6,5% (69/1066; IC 95%: 0,051–0,081) du déficit en G-6-PD a été observée respectivement chez les hommes et les femmes dans cette revue systématique. Malgré la prédominance (99,8% des cas de déficients en G-6-PD) du variant G-6-PD A- 202A/376G, les variants Santamaria et Betica Selma ont été identifiées au Burkina Faso.Indépendamment de la méthode utilisée, la prévalence du déficit enzymatique était significativement plus élevée chez les hommes (2,5–20,5%) comparativement aux femmes (3,3–12,3%).ConclusionCette revue systématique suggère qu’en dépit de l’ubiquité du variant G-6-PD A- 202A/376G au Burkina Faso, il est. nécessaire de prendre en compte les variants Santamaria et Betica Selma, bien que leurs fréquences restent à préciser. Un dépistage systématique de la déficience en G-6-PD est. également nécessaire pour prévenir la survenue d’accidents hémolytiques iatrogènes notamment chez les populations les plus vulnérables au paludisme.

Diagnostic moléculaire du Cytomégalovirus (CMV), de l’herpès virus humain de type 6 (HHV6) et d’Epstein-Barr virus (EBV) par PCR en temps réel chez les femmes enceintes VIH séropositives et séronégatives à Ouagadougou, Burkina Faso

Introduction Les herpès virus EBV, CMV et HHV-6 sont des virus qui évoluent sous le modèle pandémique et sont responsables d’infections congénitales pouvant provoquer des séquelles graves chez les nouveau-nés. L’objectif de cette étude était de déterminer les prévalences de CMV, EBV et HHV-6 chez les femmes enceintes VIH(+) et VIH(-) à Ouagadougou. Méthodes Dans cette étude 200 échantillons de plasma sanguin de femmes enceintes dont 100 femmes VIH(+) et 100 femmes VIH(-) ont été diagnostiqués par PCR multiplex en temps réel pour les trois infections (EBV, CMV et HHV-6). Résultats Sur l’ensemble des 200 échantillons analysés, 18 (9,0%) étaient positifs à au moins un des trois virus, 12 (6,0%) étaient positifs au EBV, 13 (6,5%) au CMV et 12 (6,0%) positifs au HHV-6. Parmi les 18 cas d’infections, nous avons trouvé 10 cas (55,6%) de coïnfections dont 90,0% (9/10) d’infection multiple EBV/CMV/HHV6 et 10,0% de coinfection EBV/HHV6. Le taux d’infection HHVs était plus élevé chez les femmes VIH(-) que celles VIH(+) (12,0% versus 6,0%). Parmi les VIH(+), la PCR a révélé 7,1% (soit 6/85) d’infection HHVs chez celles qui n’étaient pas sous ARV contre 0% chez celles sous ARV. Conclusion Les herpès virus sont fréquents chez les femmes enceintes au Burkina Faso et pourraient constituer une menace chez ces dernières à cause des complications et des risques d’infection pour le nouveau-né.

A Decade of Follow-up and Therapeutic Drug Monitoring in HIV-2 Immunocompromised Patients at St Camille and General Lamizana Military Medical Centers, Burkina Faso, West Africa

Introduction: Development of oropharyngeal candidiasis (OPC) in HIV infected patients on highly active antiretroviral therapy (HAART) is associated with failure of antiretroviral treatment. Methods: Type (pseudomembraneous, erythematous candidiasis or angular cheilitis) and previous episodes of OPC were recorded for HIV-infected patients on HAART. CD4 cell counts, duration, regimen and adherence on HAART were compared between patients with detectable ( 1000 copies/ ml) and undetectable HIV-RNA levels. Genotypic resistance testing was performed on those with detectable viral loads. Results: Out of 45 patients with OPC n = 29, 64 had detectable HIV-RNA levels, mostly (27/29) presenting with pseudomembranous candidiasis. The 29 patients had significantly more previous episodes of OPC (55 versus 18; P, 0.0373) and higher median CD4 cell counts (75 versus 52; P < 0.001). HIV genotyping performed in 22 of the patients showed that most (19/ 22) had at least one drug resistance mutation. Majority (14/22) had at least one thymidine analogue mutation (TAM) mostly (12/ 14) presenting as multiple TAMs. Distribution of TAMs was: T215F/Y (N = 12), M41L (n = 12), L210W (n = 5), D67N (n = 4), 219 (n = 3) and 7OR (n = 2). Lamivudine associated M184V was common (n = 13). No 65R mutation was found. One patient had major PI mutations. Conclusions: Virological failure and mutli-drug resistance including TAMs should be suspected in patients on chronic HAART that present with pseudomembraneous candidiasis. Dr. EAO Dimba, Koyio LN University of Nairobi 2 Ministry of Health Kenya, van den Sanden WJM, Creugers NHJ, Merkx MAW, Stelma FF, van der Ven AJAM, Radboud University, Nijmegen Email: elizabeth.dimba@uonbi.ac.keThis study aimed to describe the demographic and clinical profile of HIV-2 infected patients follow up from 2003 to 2013 at St Camille Medical Center and General Lamizana Military Medical Center.