Our investigation resulted in the identification of 54 conserved concepts relating to host-virus interplay, describing the means by which viruses attack host defenses or modulate cellular physiology to facilitate virus replication and propagation. These common interactions were mostly discovered in the past fifty years, and turned out to be poorly described in annotated databases; they are mostly linked to the evasion of conserved acquired or innate host-defenses. The importance of host-defense processes is underlined by the sheer quantity of viruses counteracting them; one human pathway, the RIG-like receptor pathway, is interfered with in some way by at least 14 of the 32 virus families that infect vertebrates. Upon entering a host cell, viruses must deal with host innate immunity. Pathogen recognition receptors are ����foreign���� sensors triggered by molecular patterns present in most types of viruses and/or VRT752271 bacteria. Upon activation they induce signaling events that ultimately lead to a cellular antiviral state mediated in vertebrates by the production of interferons and inflammatory cytokines. Many viruses directly block signaling components of these pathways in order to prevent the establishment of the antiviral state. RIGI is a PRR activated by cytoplasmic 59-triphosphate-RNA, a type of RNA that appears in the cell cytoplasm of virus-infected cells. Upon recognition of this ligand, RIGI initiates a cascade resulting in the expression of antiviral genes and interferon beta. This induced antiviral state is potent at preventing virus replication and exit. To replicate in vertebrate cells, many RNA viruses including influenza virus, human metapneumovirus, arenavirus, or poliovirus inhibit RIGI through different strategies. The RIGI downstream effector MAVS is targeted by the hepatitis viruses A, B and C, suggesting a crucial role for MAVS in repressing these viruses in hepatocytes. Many other viruses Lasmiditan counteract downstream key effectors of the pathway through direct interaction with IRF3, IRF7 or NF-kappaB transcription factors.