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*
Department of Pathology, University of Utah, Salt Lake City, UT 84132;
Department of Veterinary Pathobiology, University of Illinois at Urbana-Champaign, Urbana, IL 61802; and
Departments of Agronomy and Statistics, Purdue University, West Lafayette, IN 47907
A spectrum of disease severity has been observed in patients with
Lyme disease, with 
60% of untreated individuals developing
arthritis. The murine model of Lyme disease has provided strong
evidence that the genetic composition of the host influences the
severity of arthritis following infection with Borrelia
burgdorferi: infected C3H mice develop severe arthritis while
infected C57BL/6N mice develop mild arthritis. Regions of the mouse
genome controlling arthritis severity and humoral responses during
B. burgdorferi infection were identified in the
F2 intercross generation of C3H/HeNCr and C57BL/6NCr mice.
Rear ankle swelling measurements identified quantitative trait loci
(QTL) on chromosomes 4 and 5, while histopathological scoring
identified QTL on a unique region of chromosome 5 and on chromosome 11.
The identification of QTL unique for ankle swelling or
histopathological severity suggests that processes under distinct
genetic control are responsible for these two manifestations of Lyme
arthritis. Additional QTL that control the levels of circulating Igs
induced by B. burgdorferi infection were identified on
chromosomes 6, 9, 11, 12, and 17. Interestingly, the magnitude of the
humoral response was not correlated with the severity of arthritis in
infected F2 mice. This work defines several genetic loci
that regulate either the severity of arthritis or the magnitude of
humoral responses to B. burgdorferi infection in mice,
with implications toward understanding the host-pathogen interactions
involved in disease development.
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