Abstract
DISAPPOINTINGLY little is known about the mechanisms of natural, genetically determined resistance to infectious agents1. Even in the simplest situation, where a single, dominant gene is responsible for resistance to a group of closely related viruses, no satisfactory explanation of the phenomenon has been offered. A case in point is the resistance towards the lethal action of a number of myxoviruses, mainly influenza A, exhibited by the inbred mouse strain A2G and attributed to the presence of the dominant gene Mx (refs 2–5). Serial virus titrations in A2G and comparable susceptible mice showed that resistance must depend on an event occurring early in the infectious process, since by day 2 after challenge virus titres were significantly lower in resistant animals2. It was conceivable that an early triggering of the immune system might exert such an effect. If this were the case, one would expect the expression of the resistance gene to be impaired in mice showing profound disturbances of their immunological apparatus. Nude mice homozygous for the gene nu (refs 6–9) show such a disturbance, mainly of the T cell system. We have therefore introduced the gene MX into nu/nu mice, and we have investigated the progeny from appropriate crosses for the phenotypic expression of resistance to neurotropic influenza virus.
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