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Influence of Host Genes on the Outcome of Murine Lymphocytic Choriomeningitis Virus Infection

A Model for Studying Genetic Control of Virus-Specific Immune Responses

  • Chapter
The Arenaviridae

Part of the book series: The Viruses ((VIRS))

Abstract

One of the most important challenges in pathogenesis is to understand the influence of host genes on disease susceptibility. It is an attractive hypothesis to geneticists that the existence of extensive polymorphisms within populations implies that various alleles confer certain selective advantages for survival under particular evolutionary pressures. Thus, it is not surprising that when the extensive polymorphism at HLA loci (the designation for major histocompatibility complex of genes, MHC, in humans) was discovered, geneticists examined a variety of diseases for possible associations with one or more alleles at this complex of loci. Further impetus for these studies was the observation by Lilly and coworkers (1964) that in mice the H-2 complex (the designation for MHC in mice) controlled susceptibility to viral leukemogenesis. Unfortunately, the most striking finding in the majority of ensuing studies on resistance to infectious disease, in both men and mice, was how little disease resistance is influenced by MHC (Brinton and Nathanson, 1981; Clatch et al., 1987; Klein, 1986). A rare exception is the finding of two HLA types frequent among West Africans being associated with resistance to severe malaria (Hill et al., 1991). This is in contrast to the well-known associations between HLA and many autoimmune diseases (Tiwari and Terasaki, 1985). This correlation is quite understandable since until recently there was virtually no selection against noninfectious diseases, probably because people died before the diseases could develop (Klein, 1986). Although this is not the case today, autoimmune diseases still do not appear to exert any selective pressure on the population because most of them become apparent after the age of reproduction. Even at this time, the development of disease is basically a statistical risk. This could be due to multigenic effects (see below) or the need for exposure to a triggering factor (even in monozygous twins there is discordance, Tiwari and Terasaki, 1985). In addition, in almost no case do we know the etiological agent(s) responsible for an HLA-associated disease. As Klein (1986) states, “In fact, at the present stage, the study of HLA-associated diseases has about the same value to medicine as beetle counting had to zoology 200 years ago.”

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Authors and Affiliations

  1. Institute of Medical Microbiology and Institute of Experimental Immunology, University of Copenhagen, Copenhagen N, DK-2200, Denmark

    A. Randrup Thomsen

  2. Department of Biology, Rensselaer Polytechnic Institute, Troy, New York, 12181, USA

    Charles J. Pfau

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  1. A. Randrup Thomsen
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  2. Charles J. Pfau
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  1. University of Wisconsin Medical School, Madison, Wisconsin, USA

    Maria S. Salvato

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© 1993 Springer Science+Business Media New York

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Thomsen, A.R., Pfau, C.J. (1993). Influence of Host Genes on the Outcome of Murine Lymphocytic Choriomeningitis Virus Infection. In: Salvato, M.S. (eds) The Arenaviridae. The Viruses. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-3028-2_12

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  • DOI: https://doi.org/10.1007/978-1-4615-3028-2_12

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