1978
DOI: 10.1128/iai.19.2.583-588.1978
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Host Defenses in Experimental Scrub Typhus: Genetics of Natural Resistance to Infection

Abstract: Genetic resistance to lethal infection with Rickettsia tsutsugamushi was studied in over 30 inbred strains, inbred hybrids, and outbred stocks of mice. Inbred mice infected intraperitoneally with the Gilliam strain of R. tsutsugamushi

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Cited by 98 publications
(85 citation statements)
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“…Subsequent protection comes from the development of a specific immune response that usually depends on T cells (1). This division of labor does not easily account for the host response to RT, a Gram-negative intracellular bacterium that is the etiologic agent of human scrub typhus (5). This model of bacterial infection has been studied extensively because resistance to the lethal effects of acute infection is under unigenic dominant control by the Ric locus (5).…”
Section: Discussionmentioning
confidence: 99%
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“…Subsequent protection comes from the development of a specific immune response that usually depends on T cells (1). This division of labor does not easily account for the host response to RT, a Gram-negative intracellular bacterium that is the etiologic agent of human scrub typhus (5). This model of bacterial infection has been studied extensively because resistance to the lethal effects of acute infection is under unigenic dominant control by the Ric locus (5).…”
Section: Discussionmentioning
confidence: 99%
“…This division of labor does not easily account for the host response to RT, a Gram-negative intracellular bacterium that is the etiologic agent of human scrub typhus (5). This model of bacterial infection has been studied extensively because resistance to the lethal effects of acute infection is under unigenic dominant control by the Ric locus (5). Susceptible mouse strains (Ric') allow local and systemic bacterial growth during the first week of RT infection and die within 10-12 d. By contrast, RICK strains show minimal levels of bacterial infection over the first week and survive infection (37,40).…”
Section: Discussionmentioning
confidence: 99%
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“…The lpr gene does not map to the centromere end of chromosome 17 and thus is not associated with the murine major histocompatibility complex. The relationship of the gene to other non-H-2 loci reported to influence susceptibility to Leishmania donovani(Bradley et al 1979), Salmonella typhimurium(Plant & Glynn 1979) and Rickettsia tsutsugamushi(Groves et al 1980) has not been investigated, but preliminary data indicate that it is not linked to these loci. Susceptibility to common pathogens of mice is not influenced by the presence of the gene and survival times of MRL/MpJ-lpr/lpr and MRL/MpJ-+/+ animals following various doses of gamma irradiation, with or without bone marrow reconstitution, are similar (Murphy &…”
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confidence: 99%