Background. The presence of a genetic factor in the determination of l
eprosy has long been debated. This study tests whether the HLA-linked
control of susceptibility to leprosy and/or for the types of leprosy c
ould be confirmed. Materials and Methods. In 15 multicase families, th
e method of DeVries et al., 1976, was used to detect nonrandom segrega
tion of parental HLA haplotypes in their affected and healthy siblings
. Linkage analyses, for two and three alleles were performed by the co
mputer program LIPED, Results. For the affected siblings, the segregat
ions of the parental HLA haplotype were significantly nonrandom from t
he healthy parents and random from the affected parents, indicating th
at affected siblings were sharing their HLA haplotypes (segregated fro
m the healthy parents) more than expected. The segregations to the hea
lthy siblings from both the healthy and affected parents were random.
Healthy siblings inherited the haplotypes shared among the leprosy sib
lings randomly as expected. There were excess DR(2)/DR(2) homozygote i
ndividuals among tuberculoid siblings. The highest rod score was achie
ved when we considered our suggested three-alleles model for the susce
ptibility to the different types of leprosy. Conclusions. A closely HL
a-linked gene on chromosome number 6 with multiple alleles (3 or more)
in recombination fraction between 0.05 and 0.1 with 70 to 100% penetr
ance may be responsible for the susceptibility to the different types
of leprosy, whereas the susceptibility to leprosy per se maybe the res
ponsibility of non-HLA linked gene/s. DR(2)/DR(2) homozygote individua
ls may be relatively at high risk of developing leprosy or tuberculoid
leprosy.