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Herpes simplex  encephalitis (HSE) is a fatal infection of the central nervous system (CNS) predominantly caused by  Herpes simplex  virus type 1. Factors regulating the susceptibility to HSE are still largely unknown. To identify host gene(s) regulating HSE susceptibility we performed a genome-wide linkage scan in an intercross between the susceptible DA and the resistant PVG rat. We found one major quantitative trait locus (QTL),  Hse1 , on rat chromosome 4 (confidence interval 24.3–31 Mb; LOD score 29.5) governing disease susceptibility. Fine mapping of  Hse1  using recombinants, haplotype mapping and sequencing, as well as expression analysis of all genes in the interval identified the calcitonin receptor gene ( Calcr ) as the main candidate, which also is supported by functional studies. Thus, using unbiased genetic approach variability in  Calcr  was identified as potentially critical for infection and viral spread to the CNS and subsequent HSE development.

plos pathogens

The Calcitonin Receptor Gene Is a Candidate for Regulation of Susceptibility to Herpes simplex Type 1 Neuronal Infection Leading to Encephalitis in Rat