1887

Abstract

Summary

The genetics of natural resistance to the development of latent infection in the trigeminal ganglia of mice inoculated in the lip with herpes simplex virus type 1 (HSV-1) was examined. Based on coefficients of a logistic regression relating latency to strain and HSV-1 concentration, inbred strains of mice formed a continuum of resistance ranging from most resistant (C57BL/6J) to most susceptible (PL/J). When these results were analysed along with latency data derived from studies employing a non-fatal concentration of HSV-1, three subpopulations were identified among these strains: resistant (C57BL/10J, BALB/cByJ, C57BL/6J), moderately resistant (DBA/2J, SWR/J, A/J, AKR/J, DBA/1J) and susceptible (PL/J, LP/J, CBA/J). Results from F1 hybrids between resistant and moderately resistant strains (B6D2F1/J, B6AF1/J) and between resistant and susceptible strains [(C57BL/6J × CBA/J)F1, (C57BL/6J × LP/J)F1)] indicated that resistance is dominant. Data from both inbred and congenic strains failed to show an association between H-2 and resistance to the development of a latent infection. Studies of mortality also indicated that a continuum was present, with C57BL/10J, C57BL/6J and DBA/1J being most resistant and PL/J mice most susceptible. When inbred strains were categorized on the basis of resistance to the development of latent infection and mortality, five groups could be identified. Group A are strains resistant to both mortality and latency (C57BL/6J, C57BL/10J, DBA/1J) while group B consists of one strain (BALB/cByJ) intermediate in resistance to mortality but resistant to latency. Group C are strains intermediate in resistance to mortality and susceptible to latency (LP/J, CBA/J) while Group D are strains susceptible to mortality and intermediate in susceptibility to latency (AKR/J, SWR/J, DBA/2J). Group E consists of one strain (PL/J) susceptible to both mortality and latency. These results indicate that host factors play an important role in the establishment of latent infection .

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1986-04-01
2022-01-21
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