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J Gen Virol. 1986 Apr;67 ( Pt 4):613-21.

Genetics of natural resistance to herpes simplex virus type 1 latent infection of the peripheral nervous system in mice.


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 X CBA/J)F1, (C57BL/6J X 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 in vivo.

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