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 . 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).