¹Department of Molecular and Cell Biology, The University of California Berkeley, Berkeley, CA, USA

Correspondence: Professor J Rine, Department of Molecular and Cell Biology, The University of California Berkeley, 16 Barker Hall, Berkeley, CA 94720-3202, USA. E-mail: jrine@berkeley.edu

Received 12 February 2007; Revised 23 May 2007; Accepted 29 May 2007; Published online 12 July 2007.

Abstract

The pathogenic fungus Histoplasma capsulatum causes disease ranging from mild to fatal in healthy and immunocompromised humans. Infection rates reach 80% in endemic areas, including the Midwestern United States. We used inbred mice to identify a 300-fold difference in fungal burden. A/J mice showed lower fungal burden and morbidity than C57BL/6J mice, a reversal of the trend observed for many bacterial pathogens. We mapped the differences in fungal burden to discrete locations on chromosomes 1, 6, 15 and 17 with high significance. Substitution of a single resistant chromosome 17 onto the susceptible background was sufficient to lower fungal burden. These loci will allow dissection of the fungal-specific immune program.