This latest observation is in accordance with previous virus-host

This latest observation is in accordance with previous virus-host interactome features [11, 12, 23]. Furthermore, we found that a total of 47 cellular proteins (39%)

out of 120 are cellular targets for other viruses as well, including HIV, herpes, hepatitis C and papilloma viruses (Additional file 7, exact Fisher test, p-value = 1, 2.10-12). This observation reinforces our findings since different viruses, and possibly other pathogens, are expected to interact with common cellular targets as a consequence of possible common strategies adopted by viruses for infection selleck and replication [23]. Table 3 Topological analysis of the human host-flavivirus protein-protein interaction network Data set Nb of proteins Degree Betweenness (10e-4) Human interactome 10707 10, 43 1.30 Human proteins targeted by NS3 or NS5 of Flavivirus 108 22.93 4.02 We investigated the topological properties of the 108 connected identified human host proteins in comparison with all the human

proteins, which constitute the human interactome. For each dataset, the number of proteins followed by the computed average values of degree and betweenness are given. Cellular functions targeted by flavivirus We then performed an enrichment analysis using Gene Ontology (GO) database on the 120 proteins targeted by the flaviviruses in order to characterize the cellular functions significantly over-represented in the pool of proteins interacting with the flavivirus NS3 and NS5 proteins. Briefly, each cellular protein identified in our analysis and listed in the GO database click here ROS1 was ascribed with its GO features. For each annotation term, a statistical analysis evaluated a putative significant over-representation of this term in our list of proteins compared to the complete list of the human annotated proteins. The most significantly over-represented GO annotation terms are listed in Table 4. It is noteworthy that among the

enriched functions identified, some are associated with already known function of NS3 and NS5 viral proteins namely RNA binding and viral Linsitinib reproduction (Table 4, molecular function). One may thus put forward the hypothesis that among the cellular proteins listed for these two particular processes some might be key cellular partners for the viral life cycle. We also identified structural components of the cytoskeleton as cellular partners of NS3 and NS5 and we will discuss their putative implication in the viral infectious cycle thereafter in the discussion (Table 4, cellular component). Finally, our analysis revealed that the flaviviruses interact with cellular proteins involved in the Golgi vesicle transport and in the nuclear transport, suggesting that the NS3 and NS5 proteins might be able to interfere with these two cellular functions (Table 4, biological process).

37, P<0 02) and non-cloned control pigs (r=0 45, P<0 006) (Figure

37, P<0.02) and BIBW2992 in vitro non-cloned control pigs (r=0.45, P<0.006) (Figure 4C and D, respectively). Additional figure shows the changes in the relative abundance of Firmicutes and Bacteroidetes during weight-gain (See Additional file 2). Discussion In order to establish a better understanding of the underlying causes of obesity and the effect of obesity on different body sites, the cloned pigs and non-cloned control pigs employed for our study were also investigated in regard to their immunological [28], metabolomics [22] and phenotypic characters

[9]. In this study, we investigated the gut microbiota AZD5363 order of both cloned and non-cloned control pigs by T-RFLP and found that the gut microbiota within a group of five obese clones was neither more similar nor more diverse than the microbiota within a group of six obese non-cloned control pigs of the same sex and genetic background. The metabolomic phenotyping [9] of these obese cloned and non-cloned control pigs showed that the phenotype of the cloned

pigs was different from the phenotype of non-cloned control pigs [9] and that the inter-individual variation amongst these cloned pigs was not less than the inter-individual variation of the non-cloned control pigs that were siblings [22]. Hence, based on these and the findings presented Bafilomycin A1 in the current paper it would appear that the cloned pigs do not have identical phenotypes or less inter-individual variation than conventional non-cloned pigs. One explanation for these results could be that in cloning by somatic cell nuclear transfer the animals inherit maternal mitochondrial DNA and even though they have the same somatic DNA, the cloned pigs possess altering Sitaxentan phenotypes due to the maternal mitochondrial DNA effect [9]. This raises the question of whether cloned animals are more suitable animal models than conventional non-cloned animals. The heritable component of an individual and its effect on the microbial community have been investigated before in several human studies; in particular

MZ twins have been investigated to minimize the genetic influence in order to get a better understanding of the role of obesity on gut microbiota [3]. When designing an experimental model for gut microbiota related studies, it is important to remove the large variability in the microbial community across individuals, making it necessary to use larger number of animals for valid statistical analysis and interpretation. Therefore, cloned animals could have the potential of becoming good models, by reducing the number of animals needed for an experimental study and providing a less variable population, however, more optimization is needed to improve the quality of the cloned animals.

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