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Introduction et but de l’etude Les donnees sur les habitudes alimentaires d’une population tirees d’etudes epidemiologiques sont la principale source d’informations dans l’etablissement des lignes directrices nutritionnelles. Or, les methodes d’evaluation alimentaire actuelles sont autodeclarees et sontcritiquees severement en raison d’erreurs systematiques [1] . Il est donc urgent de developper de nouvelles approches evaluatives de l’alimentation afin d’en arriver a des recommandations nutritionnelles ayant plus d’impact sur la sante cardiometabolique des populations. L’etude du metabolome alimentaire, soit les substrats et intermediaires issus des reactions biochimiques liees aux aliments, s’avere une approche prometteuse [2] . Notre objectif est d’identifier la signature metabolomique d’une diete mediterraneenne (Med) a partir d’echantillons sanguins obtenus dans le cadre d’etudes controlees. Notre hypothese est qu’il existe une signature metabolomique unique de la diete Med. Materiel et methodes Un total de 96 hommes et femmes avec au moins une composante du syndrome metabolique ont participe a deux etudes d’alimentation controlees. Dans la premiere [3] , 70 participants ont recu des conseils afin d’adopter une diete fidele aux recommandations nutritionnelles pendant 4 semaines (diete sante). Puis, ils furent nourris d’une diete Med pendant 4 semaines. Dans la seconde etude [4] , 26 hommes furent nourris d’une diete nord-americaine, puis d’une diete Med pendant 5 semaines chacune. Les apports alimentaires sont objectivement mesures. Les metabolites, proteines et lipides ont ete extraits des echantillons sanguins par une methode MPLEx. La fraction metabolite fut analysee par chromatographie en phase liquide/spectrometrie de masse. Resultats et analyse statistique Le traitement des donnees massives fut realise grâce a un algorithme d’apprentissage automatique. L’apprentissage automatique a identifie des metabolites dont la nature est coherente avec les aliments fournis de la diete Med. Une analyse de type arbre decisionnel a produit des predictions basees sur les metabolites supposes identifies. Lors des tests utilisant les donnees de la premiere etude (30 replications multiples), l’exactitude moyenne (±ecart-type) concernant la prediction de la diete des participants–soit la diete sante en comparaison a la diete Med–fut de 92,9 ± 4,2 %. Dans le cas de la deuxieme etude, les metabolites supposes ont predit la diete des participants–soit une diete Med ou nord-americaine–avec une exactitude moyenne de 99,1 ± 2,7 %. Conclusion Des metabolites supposes coherents avec les aliments fournis de la diete Med predisent avec une exactitude elevee l’observance a court terme de cette diete dans le contexte de projets controles. Prochainement, examiner la plausibilite biologique des metabolites identifies et evaluer la fraction lipidique permettra de mieux caracteriser un metabolome propre a l’alimentation Med.

BACKGROUND In 2017, the Democratic Republic of the Congo (DRC) recorded its eighth Ebola virus disease (EVD) outbreak, approximately 3 years after the previous outbreak. METHODS Suspect cases of EVD were identified on the basis of clinical and epidemiological information. Reverse transcription-polymerase chain reaction (RT-PCR) analysis or serological testing was used to confirm Ebola virus infection in suspected cases. The causative virus was later sequenced from a RT-PCR-positive individual and assessed using phylogenetic analysis. RESULTS Three probable and 5 laboratory-confirmed cases of EVD were recorded between 27 March and 1 July 2017 in the DRC. Fifty percent of cases died from the infection. EVD cases were detected in 4 separate areas, resulting in > 270 contacts monitored. The complete genome of the causative agent, a variant from the Zaireebolavirus species, denoted Ebola virus Muyembe, was obtained using next-generation sequencing. This variant is genetically closest, with 98.73% homology, to the Ebola virus Mayinga variant isolated from the first DRC outbreaks in 1976-1977. CONCLUSION A single spillover event into the human population is responsible for this DRC outbreak. Human-to-human transmission resulted in limited dissemination of the causative agent, a novel Ebola virus variant closely related to the initial Mayinga variant isolated in 1976-1977 in the DRC.

Penicillin is a bactericidal antibiotic that inhibits the synthesis of the peptidoglycan by targeting penicillin-binding proteins. This study aimed to assess through transcriptional profiling the stress response of S. pneumoniae strains after exposure to lethal penicillin concentrations to understand further the mode of action of penicillin. Two experimental designs (time-course and dose-response) were used for monitoring the effect of penicillin on the transcriptional profile. The expression of some genes previously shown to be modulated by penicillin was altered, including ciaRH, pstS and clpL. Genes of the glnRA and glnPQ operons were among the most downregulated genes in the three strains. These genes are involved in glutamine synthesis and uptake and LC-MS work confirmed that penicillin treatment increases the intracellular glutamine concentrations. Glutamine conferred a protective role against penicillin when added to the culture medium. Glutamine synthetase encoded by glnA catalyses the transformation of glutamate and ammonium into glutamine and its chemical inhibition by the inhibitor L-methionine sulfoximine is shown to sensitize S. pneumoniae to penicillin, including penicillin-resistant clinical isolates. In summary, a combination of RNA-seq and metabolomics revealed that penicillin interferes with glutamine metabolism suggesting strategies that could eventually be exploited for combination therapy or for reversal of resistance.

The enhancer region in the human immunodeficiency virus type 1 (HIV-1) 5'-long terminal repeat (LTR) is very important for viral transcription. This promoter sequence binds both nuclear factor-kappaB and NFAT, two important modulators of HIV-1 gene expression. Previous studies have indicated that the enhancer regions of the different HIV-1 clade LTRs differ in their number of NF-kappaB-binding sites. In this study, we have compared the activation potential of the different HIV-1 clade and HIV-2 LTRs and assessed their interaction with NFAT and NF-kappaB. In T-cell lines and primary CD4(+) T-cells, the results showed that the HIV-1 clade E LTR (with a single NF-kappaB-binding site) was the weakest LTR regardless of the tested activators, whereas the HIV-2 LTR was the most responsive LTR. The clade E enhancer region was also demonstrated to be the weakest enhancer region in transfection experiments with luciferase reporter-based vectors. Electrophoretic mobility shift assays with extracts from activated CD4(+) T-cells indicated that, although NF-kappaB and NFAT bound all enhancers, HIV-1 clade E and HIV-2 LTR enhancers were poor binding targets for these two factors. Weak NFAT binding to clade E enhancers was also confirmed using NFAT1-expressing 293T cells in competition experiments. We have also shown the absence of interaction of NF-kappaB or NFAT with the third NF-kappaB repeat present in clade C. However, the clade C enhancer bound NFAT more efficiently than all other enhancer regions tested. Our results hence demonstrate for the first time that differences in the binding of NF-kappaB and NFAT to the enhancer regions could be responsible for some of the observed variation in HIV-1 clade LTR activation, whereas HIV-2 LTR activation seems mostly independent of these interactions.

Respiratory virus infections are a major health concern and represent the primary cause of testing consultation and hospitalization for young children. We developed and compared two assays that allow the detection of up to 23 different respiratory viruses that frequently infect children. The first method consisted of single TaqMan quantitative real-time PCR assays in a 96-well-plate format. The second consisted of a multiplex PCR followed by primer extension and microarray hybridization in an integrated molecular diagnostic device, the Infiniti analyzer. Both of our assays can detect adenoviruses of groups A, B, C, and E; coronaviruses HKU1, 229E, NL63, and OC43; enteroviruses A, B, C, and D; rhinoviruses of genotypes A and B; influenza viruses A and B; human metapneumoviruses (HMPV) A and B, human respiratory syncytial viruses (HRSV) A and B; and parainfluenza viruses of types 1, 2, and 3. These tests were used to identify viruses in 221 nasopharyngeal aspirates obtained from children hospitalized for respiratory tract infections. Respiratory viruses were detected with at least one of the two methods in 81.4% of the 221 specimens: 10.0% were positive for HRSV A, 38.0% for HRSV B, 13.1% for influenzavirus A, 8.6% for any coronaviruses, 13.1% for rhinoviruses or enteroviruses, 7.2% for adenoviruses, 4.1% for HMPV, and 1.5% for parainfluenzaviruses. Multiple viral infections were found in 13.1% of the specimens. The two methods yielded concordant results for 94.1% of specimens. These tests allowed a thorough etiological assessment of respiratory viruses infecting children in hospital settings and would assist public health interventions.