| First Author | Stadnisky MD | Year | 2009 |
| Journal | Immunogenetics | Volume | 61 |
| Issue | 11-12 | Pages | 755-64 |
| PubMed ID | 19820922 | Mgi Jnum | J:156908 |
| Mgi Id | MGI:4421647 | Doi | 10.1007/s00251-009-0400-0 |
| Citation | Stadnisky MD, et al. (2009) NK gene complex and chromosome 19 loci enhance MHC resistance to murine cytomegalovirus infection. Immunogenetics 61(11-12):755-64 |
| abstractText | An H-2(k) MHC locus is critical for murine cytomegalovirus (MCMV) resistance in MA/My mice and virus control is abolished if H-2(k) is replaced with H-2(b) MHC genes from MCMV-susceptible C57L mice. Yet, H-2(k) resistance varies with genetic background; thus, modifiers of virus resistance must exist. To identify non-MHC resistance loci, spleen and liver MCMV levels and genome-wide genotypes were assessed in (C57L x MA/My) and (MA/My x C57L) F(2) offspring (representing 550 meioses). Significantly, a non-Mendelian frequency of MHC genotypes was observed for offspring of the latter cross. Quantitative trait loci (QTL) and their interaction potential in MCMV resistance were assessed in R/qtl; QTL on chromosomes 17, 6, and 19 affected MCMV levels in infected animals. A chromosome 6 QTL was linked with the NK gene complex and acted in an additive fashion with an H-2(k) MHC QTL to mitigate spleen MCMV levels. We provide biological confirmation that this chromosome 6 QTL provided MCMV control independent of H-2(k) via NK cells. Importantly, both chromosome 6 and 19 QTLs contribute to virus control independent of H-2(k). Altogether, MHC and non-MHC MCMV-resistance QTL contribute in early resistance to MCMV infection in this genetic system. |
