results suggest that Hsp90 inhibitors prevent EBV transformation of primary T cells, and that even established LCLs are very susceptible to the toxic effect of Hsp90 inhibitors. In addition, EBV may continue in nonreplicating memory B cells without the EBNA1 expression. Ergo, clinical studies is likely to be needed to measure the potential of (-)-MK 801 these drugs for different types of EBV caused diseases. Alternative strategies have already been developed that target mobile elements, to counter-act this limitation. We hypothesized that such an strategy may be helpful to determine broad spectrum antivirals. The influenza A virus was used as a model for its viral diversity and because of the need to produce therapies against infections as recently underlined by the H1N1 pandemic. We proposed to spot a gene expression signature associated with infection by various influenza A virus subtypes which will allow the identification of potential anti-viral drugs with a broad anti influenza spectrum of activity. We examined the cellular gene expression a reaction to infection with five different human and avian influenza A virus strains Endosymbiotic theory and determined 300 genes as differentially expressed between infected and non infected samples. One of the most 20 dysregulated genes were used to screen the map, a database of drug associated gene expression profiles. Prospect antivirals were then identified by their inverse correlation for the query signature. We hypothesized that such molecules would stimulate a negative mobile environment for influenza virus replication. Ten likely antivirals including ribavirin were recognized and their results were examined in vitro on five influenza A strains. Influenza viral growth was inhibited by six of the molecules. The new pandemic H1N1 virus, which wasn’t used to define the gene expression signature of infection, ATP-competitive ALK inhibitor was restricted by five from the ten recognized elements, demonstrating that method can donate to distinguishing new vast anti influenza agents acting on cellular gene expression. The identified infection signature genes, the expression of which are altered upon infection, can encode proteins active in the viral life cycle. This is actually the first study showing that gene expressionbased assessment may be used to recognize antivirals. Such an method might accelerate drug development and be extended to other infections. Anti-viral drug development is based on two approaches: i) the conventional approach of suppressing the action of a viral enzyme which regularly leads to the emergence of drug resistant worms due to viral genomic variability and ii) the newer approach of targeting cellular factors that are needed for viral replication.