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PubMed1987

[Immunogenetics of multiple sclerosis].

The interaction between environmental factors and genetic susceptibility causes multiple sclerosis. In some ethnic groups this disease is rare. The family incidence varies from 6 to 12%. Analysis of twins shows a concordance two fold higher in homozygous twins. The transmission of such a genetic susceptibility cannot be explained by means of an usual genetical model. In Caucasoids, an association exists between MS and HLA A3, B7 and DR2 antigens. However this association is not always found and can be different from one population to another one. The mechanisms of the association are unknown: either the HLA haplotype supports the disease susceptibility but family segregation studies are unconvincing, or this susceptibility is due to the interaction of several genic complexes, a few of which linked to HLA region. An etiological heterogeneity of MS has also been suggested.

Disease Susceptibility↗
PubMed1988

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.

Animals↗