Abstract

If viruses, by their variety, distribution, potential virulence and sheer inexhaustibility, present a permanent threat to the well-being of organisms, one might wonder why good health still exists. Yet healthy organisms do exist, though not because they simply evade the tireless viral intruders, but because they constantly mobilize potent defense forces. In vertebrates, T and B cell-mediated immunity is usually credited with being of prime importance in antiviral defense, but often, the first hurdles viruses have to clear are not antibodies and T cells but the flow of mucus, the acidity of the stomach, the paucity of appropriate cellular virus receptors, or the inadequacy of a synthetic machinery that viruses need to usurp for their replication. These hurdles are host defense mechanisms no less important for the homeostasis of health than the specific immune system; they are placed at various levels and make the interplay between virus and host a notoriously complex affair. The method of choice to elucidate such defense mechanisms at the molecular level is the analysis of genetic variants in which these defense forces are altered. Although such variants abound from plants (FRASER 1990) to mammals (for mice, see GREEN 1989), only a few of the associated genes have been isolated or characterized (for example, DÉzÉlÉe et al. 1989; Dveksler et al. 1991; Yokomori and Lai 1992; NÉdellec étal. 1994; Bureau et al. 1993), most likely because many of these variants are multigenic in origin and difficult to analyze.KeywordsTransgenic MouseInfluenza VirusAntiviral ActivityVesicular Stomatitis VirusMouse Hepatitis VirusThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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