Table III.

Homozygosity for the G2M*n allele and the GM*b;f;n haplotype confers resistance to invasive infection in C2D

G2M AllotypebG2M(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)7c2d0d1e011
Group 2 (n = 7)060100
Group 3 (n = 12)045300
Group 4 (n = 13)242401
Total (n = 44)20.9%37.2%16.3%18.6%2.3%4.7%
Controls (n = 430)f19.3%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 ).