This general purpose strain shares a common origin with C3H/HeJ and C3H/HeOuJ. Unlike C3H/HeJ, it carries a normal allele at the Tlr4 locus, but is homozygous for Pde6b^rd1, which causes retinal degeneration. This C3H subline lacks the nob5 allele of Gpr179 (Chang, 2015). C3HeB/FeJ inbred mice have been found to be extremely susceptible to virulent Mycobacterium tuberculosis. They develop pulmonary tuberculosis and die within 25-28 days of infection with 10⁵ CFU of Erdman strain of M. tuberculosis (Kramnik et al, 1998). Several QTL have been identified that contribute to the M. tuberculosis susceptibility (Sissons et al., 2009). The QTL susceptibility to tuberculosis 1 (sst1) on Chromosome 1, mapped to a locus that includes the Sp110 gene, which was shown to have variable copy number in C3HeB/FeJ and comparatively decreased expression subsequent to TB infection. Transgenic expression of Sp110 in macrophages increased resistance to TB in C3HeB/FeJ (Pan et al., 2005, Kramnik, 2008). C3HeB/FeJ has also been found to be susceptible to infection by Chlamydia pneumoniae and Listeria monocytogenes and that susceptibility also maps in part to the sst1 locus (Boyartchuk et al., 2004, He et al., 2013). These mice have also been found to be susceptible to Salmonella typhimurium infection (Eisenstein et al., 1982). In response to kainic acid this inbred strain has a low dose tolerance, high rate of induced seizure duration and severity, and high induced mortality rate. None survive induced status epilepticus, and just prior to severe seizures the mice display hyperactivity and running behavior (McKhann et al., 2003).