With the availability of complete DNA sequences for many prokaryotic and eukaryotic genomes, and soon for the human genome itself, it is important to develop reliable proteome-wide approaches for a better understanding of protein function. As elementary constituents of cellular protein complexes and pathways, protein-protein interactions are key determinants of protein function. Here we have built a large-scale protein-protein interaction map of the human gastric pathogen Helicobacter pylori. We have used a high-throughput strategy of the yeast two-hybrid assay to screen 261 H. pylori proteins against a highly complex library of genome-encoded polypeptides. Over 1,200 interactions were identified between H. pylori proteins, connecting 46.6% of the proteome. The determination of a reliability score for every single protein-protein interaction and the identification of the actual interacting domains permitted the assignment of unannotated proteins to biological pathways.

No abstract

No abstract

BackgroundThe development of polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique for species identification among patients presenting leishmaniasis allowed to better determine the main circulating species in French Guiana.MethodsA descriptive study of the Leishmania species was identified, and their spatiotemporal distribution was conducted using patient records between 2006 and 2013, with 1017 new cases of leishmaniasis diagnosed. Identification was realized by PCR-RFLP on 745 cases.ResultsThe average proportions for different species were 86.2% for Leishmania (Vianna) guyanensis; 9.7% for Leishmania (Vianna) braziliensis; 2.8% for Leishmania (Leishmania) amazonensis; and 1.3% for Leishmania (Vianna) lainsoni, and no case of Leishmania (Vianna) naiffi was identified. Over this period, the proportion of cases due to L. (V.) braziliensis seemed to increase from 8.9% in 2006 to 13.0% in 2013 notably near the gold mining zones.ConclusionsThe use of molecular tools has transformed the view of the local epidemiology of cutaneous leishmaniasis in French Guiana.

BackgroundPrevious studies have stressed the genetic divergence and high pathogenicity of strains of T. gondii from French Guiana. Although strains from coastal, human adapted environments (so called anthropized) resemble those found in other regions of the Caribbean, strains collected from inland jungle environment are genetically quite diverse. To better understand the composition of these distinct strain types, we undertook a more in depth analysis of T. gondii strains from French Guiana including profiling of chromosome 1a (Chr1a), which is often shared as a single monomorphic haplotype among lineages that are otherwise genetically distinct.Methodology/Principal FindingsComparison of intron sequences from selectively neutral genes indicated that anthropized strains were most closely related to clonal type III strains from North America, although wider RFLP analysis revealed that they are natural hybrids. In contrast, strains isolated from the jungle were genetically very diverse. Remarkably, nearly all anthropized strains contained the monomorphic version of Chr1a while wild stains were extremely divergent. The presence of the monomorphic Chr1a strongly correlated with greater transmission in domestic cats, although there were several exceptions, indicating that other factors also contribute. Anthropized strains also varied in their virulence in laboratory mice, and this pattern could not be explained by the simple combination of previously identified virulence factors, indicating that other genetic determinants influence pathogenicity.Conclusions/SignificanceOur studies underscore the marked genetic separation of anthropized and wild strains of T. gondii in French Guiana and provide additional evidence that the presence of Chr1a is associated with successful expansion of widely different lineages within diverse geographic areas. The predominance of Chr1a among strains in the anthropized environment suggests that it may confer an advantage for transmission in this environment, and thus potentially contribute to the spread of pathogenecity determinants.