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Introduction Le VIH-2, endémique en Afrique de l'Ouest, est naturellement résistant aux inhibiteurs non nucléosidiques de la rétro transcriptase (INNRTI), ce qui rend difficile la prise en charge dans les pays en développement. L’objectif ici était de déterminer la prévalence de l'échec virologique au 12éme et 24éme mois (M12 et M24) de traitement antirétroviral de première ligne chez les patients infectés par le VIH-2 et d'en décrire les résistances génotypiques associées. Méthodes Il s'agit d'une étude descriptive longitudinale et prospective, durant la période de novembre 2005 à juin 2017. L'échec virologique a été défini comme toute charge virale supérieure à 50 copies/ml après 6 mois de traitement ARV à deux reprises. La recherche de mutations de résistance a été réalisée dans les régions codantes de la protéase et de la transcriptase inverse. Résultats Au total 110 patients ont été colligés, d'âge médian de 46 ans (Extrêmes 18-67) avec un ratio F/H de 2,54. À l'inclusion, la charge virale était détectable dans 44% des cas avec une médiane de 935cp/ml (Extrêmes 17-144038). Le schéma antirétroviral associait 2 INTI à 1IP dans 94% des cas. La durée médiane de suivi était estimée à 1200 jours (Extrêmes 1-3840). 94 puis 76 patients ont respectivement complété leur bilan à M12 et M24. Au suivi M24, 39 patients étaient en échec virologique soit une prévalence de 39% estimée à 33% à M12 et 11% à M24. 45% des patients avaient des résistances aux inhibiteurs nucléosidiques de la transcriptase inverse (INTI), 41% des résistances aux IP et 30% des multi résistances aux INTI et IP. Conclusion Il est impératif de rendre accessible les nouvelles classes thérapeutiques pour le traitement de sauvetage des patients infectés par le VIH-2 dans les pays à ressources limitées.

Background Hepatitis B (HB) infection is common in Mali. However, there is little information on molecular and biochemical characteristics of HB carriers. Methods A group of 1466 adult volunteers was recruited in the district of Bamako. Confirmed HB carriers were tested for HB viral load by quantitative PCR and HBV was genotyped by sequencing of HBS. Fibrosis and hepatitis activity were measured using the Fibrotest-Actitest. A mutation of TP53 at codon 249 (R249S), specific for exposure to aflatoxin, was detected in cell-free DNA extracted from plasma. Results Overall, 276 subjects were HBsAg-positive (18.8%). Among 152 subjects tested for HBV load, 49 (32.2%) had over 104 copies/mL and 16 (10.5%) had levels below the limit of detection. The E genotype was found in 91.1% of carriers. Fibrotest scores ≥ F2 were observed in 52 subjects (35.4%). Actitest scores ≥ A2 were detected in 15 subjects (10.2%) and were correlated with Fibrotest scores (p = 0.0006). Among 105 subjects tested, 60% had detectable levels of R249S copies (>40 copies/mL plasma). Conclusion Chronic HB carriage in adults in Bamako district is well over epidemic threshold. About 1/3 of carriers have moderate to severe liver fibrosis and 60% have detectable aflatoxin-related TP53 R249S mutation. These results support introduction of anti-HB therapies to reduce the progression towards severe liver disease.

In Burkina Faso as in other underdeveloped countries, access to health care in general and dermatology care in particular remains difficult. This situation puts pharmacies on the front line for providing counselling. We undertook a cross-sectional descriptive study of the pharmacies of Ouagadougou from October 1, 2002, through April 1, 2003. Our objective was to evaluate the prevalence of dermatological and cosmetic counselling. The study included 75.5% of all pharmacies and 150 service providers. Prevalence of dermatology counseling was considered moderate, as was the availability and use of dermatology products. Service providers did not know most of the common dermatology disorders and offered inappropriate advice and products. This study shows the gap between the need for counselling from pharmacies and its satisfaction. It also underlines the necessity of reorganization in this domain.

Information on the replication of viral haemorrhagic fever viruses is not readily available and has never been analysed in a comparative approach. Here, we compared the cell culture growth characteristics of haemorrhagic fever viruses (HFV), of the Arenaviridae, Filoviridae, Bunyaviridae, and Flavivridae virus families by performing quantitative analysis of cell culture supernatants by (i) electron microscopy for the quantification of virus particles, (ii) quantitative real time PCR for the quantification of genomes, and (iii) determination of focus forming units by coating fluorescent antibodies to infected cell monolayers for the quantification of virus infectivity. The comparative analysis revealed that filovirus and RVFV replication results in a surplus of genomes but varying degrees of packaging efficiency and infectious particles. More efficient replication and packaging was observed for Lassa virus, and Dengue virus resulting in a better yield of infectious particles while, YFV turned out to be most efficient with only 4 particles inducing one FFU. For Crimean-Congo haemorrhagic fever virus (CCHFV) a surplus of empty shells was observed with only one in 24 particles equipped with a genome. The complete particles turned out to be extraordinarily infectious. Background Viral haemorrhagic fevers (VHF) are caused by various haemorrhagic fever viruses (HFV), of the Arenaviridae, Filoviridae, Bunyaviridae ,a ndFlavivridae virus families. Only few laboratories specialize in the research on these agents. Basic virological info rmation on these viruses is scant and described exclusively in the frame of case reports and pathological animal models. Although some progress has been achieved concerning the interaction of these viruses with mechanisms of innate immunity [1-9] and nitrite oxide pathways (CCHFV) [7] concise information on their basic virological characteristics is limited. This type of data however is important for biosafety risk assessment purposes. Here, we present a comparative analysis of quantities of HFV in cell culture determined by electron microscopic counting, quantitative real time RT-PCR and focus forming units, which reveal some features of the replication of these viruses that have not been described before. Methods Virus propagation