Resistance to HSV-1 in the mouse is governed by two major, independently segregating, non-H-2 loci.
Earlier studies showed that genetic resistance of adult, inbred strains of mice to Herpes Simplex Virus-type 1 (HSV-1) is a dominant genetic trait. The present studies were undertaken to determine the number of genetic loci involved and whether they were found within the major histocompatibility complex, H-2, of the mouse. Challenge with HSV-1 of progeny of mice backcrossed to moderately susceptible BALB/c mice, of progeny of mice backcrossed to very susceptible A/J strain mice, and of progeny of the F-2 cross using (C57BL/6 x A/J)F1 mice indicated that two major loci were responsible for resistance. The backcrosses to BALB/c mice suggested that additional genes on this background enhanced resistance, while further backcrosses with the A/J mice indicated that other genes on the A/J background (or the lack thereof) reduced resistance. Studies with congenic mice showed that genes within the H-2 did not influence resistance or susceptibility.
D000818:Animals; D002874:Chromosome Mapping; D003433:Crosses, Genetic; D005260:Female; D005796:Genes; D008040:Genetic Linkage; D006183:H-2 Antigens / Q000235:genetics; D006561:Herpes Simplex / Q000276:immunology*; D007113:Immunity, Innate; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains / Q000235:genetics*; D018139:Simplexvirus / Q000276:immunology
D006183:H-2 Antigens