Immunogenetic influence of Igh-1 phenotype on experimental herpes simplex virus type-1 corneal infection.
Patterns of herpes simplex virus type-1 (HSV-1) infection were studied in BALB/c congenic, Igh-1 disparate murine strains to establish the influence of Igh-1 phenotype on the development of keratopathy, trigeminal ganglionic latency and keratocyte permissivity. Eighty-two percent of C.AL-20 (Igh-1d) mice, 40% of BALB/cByJ (Igh-1a) mice and 12% of the C.B-17 (Igh-1b) mice developed herpes simplex keratitis (HSK) following corneal challenge with 2.5 X 10(4) PFU HSV-1 strain KOS. While disease frequency was directly proportional to HSV-1 challenge dose, relative resistance and susceptibility patterns in the congenic mice were constant and highly significant. F1 progeny from C.AL-20 X C.B-17 matings demonstrated the HSK pattern of the C.B-17 parent suggesting that Igh-1 linked resistance to HSK is dominantly inherited. Equivalent trigeminal ganglionic latency was established following ocular HSV-1 inoculation in the three congenic Igh-1 disparate murine strains. Cultured keratocytes from the three Igh-1 disparate murine strains demonstrated equivalent in vitro permissivity to HSV-1 replication. These data illustrate a strong correlation between Igh-1 phenotype and the development of a HSK in congenic mice. The susceptibility/resistance to HSK in these mice is unrelated to trigeminal ganglionic latency or keratocyte permissivity.
Opremcak
E M
EM
Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston 02114.
Wells
P A
PA
Thompson
P
P
Daigle
J A
JA
Rice
B A
BA
Millin
J A
JA
Foster
C S
CS
D000818:Animals; D003315:Cornea / Q000166:cytology / Q000382:microbiology; D005260:Female; D005796:Genes; D007635:Keratitis, Dendritic / Q000235:genetics* / Q000276:immunology / Q000382:microbiology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D010641:Phenotype; D014779:Virus Replication