bioRxiv preprint doi: https://doi.org/10.1101/2020.09.23.310409; this version posted November 11, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. 1 Interferon receptor-deficient mice are susceptible to eschar-associated rickettsiosis Thomas P. Burke1*, Patrik Engström1, Cuong J. Tran1,2, Dustin R. Glasner2,3, Diego A. Espinosa2,4, Eva Harris2, Matthew D. Welch1* 1Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, CA, USA 2Division of Infectious Disease and Vaccinology, School of Public Health, University of California, Berkeley, Berkeley, CA, USA 3Current address: Department of Laboratory Medicine, University of California, San Francisco, San Francisco, CA, USA 4Current address: Metagenomi, Emeryville, CA, USA *email:
[email protected];
[email protected] bioRxiv preprint doi: https://doi.org/10.1101/2020.09.23.310409; this version posted November 11, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. 2 1 Abstract 2 Rickettsia are arthropod-borne pathogens that cause severe human disease worldwide. The 3 spotted fever group (SFG) pathogen Rickettsia parkeri elicits skin lesion (eschar) formation in humans 4 after tick bite. However, intradermal inoculation of inbred mice with millions of bacteria fails to elicit 5 eschar formation or disseminated disease, hindering investigations into understanding eschar- 6 associated rickettsiosis.