Date of Award
Life & Environmental Sciences
Rev. Joseph Harrington
Mink cell focus-inducing virus MCF-247 was inoculated into various strains of mice to determine whether any of these strains mount a humoral immune response to the virus. Finding that there were both responders and nonresponders, a genetic study was conducted in order to determine what controls the immune response. C57BL/6J mice (high antibody responders) and DBA/2J mice (nonresponders) were crossed and the genetics of their F1, F2 and Backcross to DBA/2J mice were followed. Indirect immunofluorescent assays determined that the F^ generation uniformly ' produced a high antibody titer when inoculated with the virus. The F2 and Backcross generations were found to have high responders (titer 80), low responders (titer 80), and nonresponders (titer 10) to the inoculated virus. All mice were inoculated as babies and were tested 1-6 months after injection. Various genotypic models were proposed for the genetic control of the immune response. It appears that at least one and possibly two genes are involved in control of the immune response. Possible association of the mouse H-2 major histocompatibility complex, shown to regulate various immune responses (12), with the immune response to inoculated MCF-247 virus was investigated. Hemagglutination tests indicated that there does not appear to be any association between the two. Rather, the immune response appears to be like that to type III pneumococcal polysaccharide, in which nonH-2 genes control the immune response (13). Possible links between the immune response gene(s) and the coat color gene b. were investigated for the purpose of aiding in the mapping of the immune response gene(s). It was determined that the two are not linked. The immune response was also determined to be a nonsexlinked trait. Further research of the immune response is indicated.
Margaris, Melchisedek, "A Genetic Study Of The Murine Humoral Immune Response To MCF-247 Virus" (1983). Life and Environmental Sciences Undergraduate Theses. 431.