Trischmann T M
Infect Immun. 1984 Dec;46(3):658-62. doi: 10.1128/iai.46.3.658-662.1984.
The inability of the BXH-2 recombinant inbred strain to limit proliferation of Trypanosoma cruzi during the first 2 weeks after infection was found to be controlled by a single locus difference between the BXH-2 strain and each of its parental strains: C3H/HeJ and C57BL/6J. In both cases, the inability to limit parasite proliferation acted like a recessive trait. The loci in the C3H and C57BL/6 strains appear to be identical since all F2 mice derived from these strains displayed the early control trait. A mutation is thus likely to have occurred in the derivation of the BXH-2 strain. The provisional designation Crz has been given to the locus in the BXH-2 strain that is responsible for its failure to control early proliferation of T. cruzi. The Crz locus is distinct from the lpr gene which has also been associated with increased levels of parasitemia early in the course of the infection.
研究发现，BXH-2重组近交系在感染后的前两周内无法限制克氏锥虫的增殖，这一现象由BXH-2品系与其亲本品系C3H/HeJ和C57BL/6J之间的单个基因座差异所控制。在这两种情况下，无法限制寄生虫增殖的性状表现为隐性性状。由于来自这些品系的所有F2小鼠都表现出早期控制性状，因此C3H和C57BL/6品系中的基因座似乎是相同的。因此，在BXH-2品系的衍生过程中可能发生了突变。BXH-2品系中负责其无法控制克氏锥虫早期增殖的基因座被暂时命名为Crz。Crz基因座与lpr基因不同，lpr基因也与感染早期寄生虫血症水平的升高有关。
