Our observations of marked intra-group variation (i.e., some animals in M1 had relatively high Hp concentrations and vice versa for some in M2) most-likely reflected differences in the degree of immune activation, for example unexpectedly high concentrations may have been related to the presence of secondary bacterial infections (27), or other comorbidities (15), while stressors (17) or immune exhaustion may have contributed to lower than expected concentrations. The gene discussed is HP; the disease is bacterial infectious disease.