A Cmv2 QTL on chromosome X affects MCMV resistance in New Zealand male mice |
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| Authors: | Marisela R Rodriguez Alyssa Lundgren Pearl Sabastian Qian Li Gary Churchill Michael G Brown |
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| Institution: | (1) Department of Microbiology, University of Virginia School of Medicine, Charlottesville, VA 22908, USA;(2) Department of Medicine, University of Virginia School of Medicine, Charlottesville, VA 22908, USA;(3) The Jackson Laboratory, 600 Main Street, Bar Harbor, ME 04609, USA;(4) Department of Internal Medicine, Division of Rheumatology, Washington University in St. Louis Medical Center, 600 South Euclid Avenue, Box 8045, St. Louis, MO 63110, USA |
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| Abstract: | NK cell-mediated resistance to viruses is subject to genetic control in humans and mice. Here we used classical and quantitative
genetic strategies to examine NK-mediated murine cytomegalovirus (MCMV) control in genealogically related New Zealand white
(NZW) and black (NZB) mice. NZW mice display NK cell-dependent MCMV resistance while NZB NK cells fail to limit viral replication
after infection. Unlike Ly49H+ NK resistance in C57BL/6 mice, NZW NK-mediated MCMV control was Ly49H-independent. Instead, MCMV resistance in NZW (Cmv2) involves multiple genetic factors. To establish the genetic basis of Cmv2 resistance, we further characterized a major chromosome X-linked resistance locus (DXMit216) responsible for innate MCMV control in NZW × NZB crosses. We found that the DXMit216 locus affects early MCMV control in New Zealand F2 crosses and demonstrate that the NZB-derived DXMit216 allele enhances viral resistance in F2 males. The evolutionary conservation of the DXMit216 region in mice and humans suggests that a Cmv2-related mechanism may affect human antiviral responses.
Electronic supplementary material The online version of this article (doi:) contains supplementary material, which is available to authorized users. |
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