Homozygosity for the G2M*n allele and the GM*b;f;n haplotype confers resistance to invasive infection in C2D
G2M Allotypeb | G2M(n,n) | G2M(n,n−) | G2M(n−,n−) | ||||
---|---|---|---|---|---|---|---|
GM Haplotype | *b;f;n/b;f;n | *b;f;n/g;a;n− | *b;f;n/*b;f;n− | *n/n− | *b;f;n−/g;a;n− | *g;a;n−/g;a;n− | *b;f;n −/*b;f;n− |
Group 1 (n = 12) | 7c | 2d | 0d | 1e | 0 | 1 | 1 |
Group 2 (n = 7) | 0 | 6 | 0 | 1 | 0 | 0 | |
Group 3 (n = 12) | 0 | 4 | 5 | 3 | 0 | 0 | |
Group 4 (n = 13) | 2 | 4 | 2 | 4 | 0 | 1 | |
Total (n = 44) | 20.9% | 37.2% | 16.3% | 18.6% | 2.3% | 4.7% | |
Controls (n = 430)f | 19.3% | 27.2% | 17.4% | 17.7% | 9.8% | 6.7% |
a The G2M(n) and G2M(n−) allotypes and the associated GM haplotypes are given in the C2D patients, who were divided into groups according to the severity of the infections (see Table I⇑).
b In 40 patients, confirmatory investigation of G2Mn and G2Mn− was performed by DNA analysis.
c p < 0.001 (Fisher’s exact test) for the homozygous presence of G2M(n) in group 1 compared with groups 2–4.
d As compared with the GMb;f;n− haplotype, the increased prevalence of the GMg;a;n− haplotype among heterozygous patients with noninvasive infections was not statistically significant (p = 0.15, Mann-Whitney U test).
e One patient could only be analyzed for G2M(n) due to lack of serum.
f The distribution of GM haplotypes in the C2D cohort did not differ (p = 0.72, CHI2 test) from that found in a previously described control population (22 ).