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During their blood meal, ticks secrete a wide variety of proteins that can interfere with their host's defense mechanisms. Among these proteins, lipocalins play a major role in the modulation of the inflammatory response. We previously identified 14 new lipocalin genes in the tick Ixodes ricinus. One of them codes for a protein that specifically binds leukotriene B4 with a very high affinity (Kd: +/-1 nM), similar to that of the neutrophil transmembrane receptor BLT1. By in silico approaches, we modeled the 3D structure of the protein and the binding of LTB4 into the ligand pocket. This protein, called Ir-LBP, inhibits neutrophil chemotaxis in vitro and delays LTB4-induced apoptosis. Ir-LBP also inhibits the host inflammatory response in vivo by decreasing the number and activation of neutrophils located at the tick bite site. Thus, Ir-LBP participates in the tick's ability to interfere with proper neutrophil function in inflammation. These elements suggest that Ir-LBP is a \"scavenger\" of LTB4, which, in combination with other factors, such as histamine-binding proteins or proteins inhibiting the classical or alternative complement pathways, permits the tick to properly manage its blood meal. Moreover, with regard to its properties, Ir-LBP could possibly be used as a therapeutic tool for illnesses associated with an increased LTB4 production.

This is the first comprehensive book on human/animal gene responses to RNA viral infections, including prevalent, emerging and re-emerging RNA viruses such as HIV, SARS-CoV, West Nile virus, influenza virus and many others. Human gene responses are reviewed by leading virologists worldwide in the following aspects: (i) the altered gene expression profiles at the transcriptional and translational levels detected with cutting-edge technologies such as cDNA microarray and proteomics; (ii) host innate and adapted immune responses to viral replication in target organs; (iii) virus-activated signal transduction pathways in cell survival, apoptosis and autophagosomal pathways; and (iv) the small interfering RNA/microRNA-mediated gene silencing pathway, a recently characterized new host defense mechanism against viral infection.