We hypothesized that any compound able to inverse the illness signature should be bad for influenza virus replication. Rilmenidine and aminobenzenesulfonamide had only a small anti-viral impact on one particular disease. Harmol and merbromin were poor inhibitors of most of the tested viruses. Midodrine and brinzolamide were Imatinib clinical trial poor to moderate inhibitors of most of the tested viruses. Needlessly to say, ribavirin was a powerful inhibitor of most tested worms. In light of the results, we consider that we’ve discovered a typical signature whose partial inversion is strong enough to prevent viral replication. We cannot exclude that some in silico selected drugs exert a possible direct influence on an activity or on a path exploited by the herpes virus. On the list of seven elements, three specifically could have this effect: ribavirin and merbromin which could both directly inhibit a viral purpose, and harmol which could inhibit a path. Harmol can be a beta carboline alkaloid of the medicinal plant, Perganum harmala L.. Several certain effects are defined Infectious causes of cancer for harmol except that it puts a psychoactive influence by inhibiting monoamine oxydase, moderately inhibits platelet aggregation by inhibiting PLCc2 and induces apoptosis in certain cell lines by activating caspase 8. PLCc2 is implicated in the protein kinase C activation route, the experience of which is crucial for influenza virus entry. Consequently its inhibition by harmol can simply result in the antiviral effect found by this compound. Moreover, activation of apoptosis might restrict viral replication. Nevertheless, three forms of evidence support our theory that the selected compounds have an antiviral effect by enhancing the host cell gene expression. First, the outcomes of our test of infection efficiencies show that none of the molecules except for merbromin had an effect on composition or function before infection. Next, the large confirmation price of the in silico chosen medicine panel validate the rational of the selection. Hedgehog pathway inhibitor Last, some elements that controlled the host cell transcription in the exact same way that influenza virus infection improved viral production. To your knowledge, modulation of the cell gene expression has never been identified to support the effects of the in silico chosen medicine, except for ribavirin. This antiviral drug with in vitro activity against both DNA and RNA viruses, has many mechanisms of action proposed to guide its antiviral effect the depletion of the intracellular GTP share by inhibition of inosine monophosphate dehydrogenase compromises the formation of progeny viral RNA, ii) the inhibition of viral RNA dependent RNA polymerase activity has been shown for hepatitis C and influenza viruses, and iii) it may act as a RNA virus mutagen producing error problem. Which components give rise to its anti influenza effect in vivo remains undetermined.