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Publication : Host defenses in experimental rickettsialpox: genetics of natural resistance to infection.

First Author  Anderson GW Jr Year  1980
Journal  Infect Immun Volume  28
Issue  1 Pages  132-6
PubMed ID  7380561 Mgi Jnum  J:24677
Mgi Id  MGI:72411 Doi  10.1128/iai.28.1.132-136.1980
Citation  Anderson GW Jr, et al. (1980) Host defenses in experimental rickettsialpox: genetics of natural resistance to infection. Infect Immun 28(1):132-6
abstractText  The genetic basis for natural resistance to lethal infection with Rickettsia akari was studied in over 25 inbred strains, inbred hybrids, and outbred stocks of mice. Inbred mice infected intraperitoneally with the Kaplan strain of R. akari demonstrated three levels of response, susceptible (C3H/HeJ), intermediate (A/HeJ, A/J, A/WySn, BALB/cDub, BALB/cJ, and SJL/J), and resistant (AKR/J, AL/N, BALB/cAnN, BALB/cNCr1BR, C3H/HeN, C57BL/6J, C57L/J, CBA/J, DBA/2J, and SWR/J). No correlation was evident between the six H-2 haplo-types tested and susceptibility to Kaplan infection. Four outbred mouse stocks, Dub: (ICR), Wrc:(ICR), Caw:(CF1), and Mai:(S) were all resistant. The F1 inbred hybrids of resistant X resistant (AKD2F1/J), resistant X intermediate (CB6F1/U), intermediate X intermediate (CAF1/J), and resistant X susceptible (C3D2F1/J) parents were all resistant. The F2 and parental backcross generations of C3H/HeJ and DBA/2J hybrids yielded ratios of resistant to susceptible mice that suggested resistance was under multigeneic control. Susceptible mice (C3H/HeJ) were capable of mounting an immune response, since prior infection with the avirulent Hartford strain of R. akari rendered them resistant to subsequent lethal challenge with the Kaplan strains.
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