Association between variant FcγRgenotypes and Kaposi's sarcoma (KS) in 2 populations of HIV-infected men
FcγR genotypes . | Population I . | Population II . | Combined populations . | |||||||||
---|---|---|---|---|---|---|---|---|---|---|---|---|
KS (n = 58) Number of patients (%) . | No KS (n = 61) . | Evidence for association P values for . | KS (n = 61) . | No KS (n = 70) . | Evidence for association P values for . | KS (n = 119) . | No KS (n = 131) . | Evidence for association P values for . | ||||
Locus . | Genotype . | Locus . | Genotype . | Locus . | Genotype . | |||||||
FcγRIIA | ||||||||||||
HH | 21 (36.8) | 12 (19.7) | 16 (26.7) | 20 (28.6) | 37 (31.6) | 32 (24.4) | ||||||
HR | 25 (43.9) | 37 (60.6) | .096 | 29 (48.3) | 33 (47.1) | .97 | 54 (46.2) | 70 (53.4) | .40 | |||
RR | 11 (19.3) | 12 (19.7) | 15 (25) | 17 (24.3) | 26 (22.2) | 29 (22.2) | ||||||
FcγRIIIA | ||||||||||||
VV | 7 (12.7) | 10 (16.7) | .55 | 9 (15.8) | 5 (7.4) | .14 | 16 (14.3) | 15 (11.7) | .55 | |||
VF | 36 (65.5) | 21 (35) | .0035 | .0011 | 36 (63.1) | 33 (48.4) | .018 | .10 | 72 (64.3) | 54 (42.2) | .00028 | .00063 |
FF | 12 (21.8) | 29 (48.3) | .0030 | 12 (21.1) | 30 (44.1) | .0065 | 24 (21.4) | 59 (46.1) | .000061 | |||
FcγRIIIB | ||||||||||||
1/1 | 11 (19.3) | 8 (13.8) | 7 (11.9) | 10 (14.7) | 18 (15.5) | 18 (14.3) | ||||||
1/2 | 21 (36.9) | 23 (39.7) | .73 | 34 (57.6) | 35 (51.5) | .77 | 55 (47.4) | 58 (46.0) | .89 | |||
2/2 | 25 (43.8) | 27 (46.5) | 18 (30.5) | 23 (33.8) | 43 (37.1) | 50 (39.7) |
FcγR genotypes . | Population I . | Population II . | Combined populations . | |||||||||
---|---|---|---|---|---|---|---|---|---|---|---|---|
KS (n = 58) Number of patients (%) . | No KS (n = 61) . | Evidence for association P values for . | KS (n = 61) . | No KS (n = 70) . | Evidence for association P values for . | KS (n = 119) . | No KS (n = 131) . | Evidence for association P values for . | ||||
Locus . | Genotype . | Locus . | Genotype . | Locus . | Genotype . | |||||||
FcγRIIA | ||||||||||||
HH | 21 (36.8) | 12 (19.7) | 16 (26.7) | 20 (28.6) | 37 (31.6) | 32 (24.4) | ||||||
HR | 25 (43.9) | 37 (60.6) | .096 | 29 (48.3) | 33 (47.1) | .97 | 54 (46.2) | 70 (53.4) | .40 | |||
RR | 11 (19.3) | 12 (19.7) | 15 (25) | 17 (24.3) | 26 (22.2) | 29 (22.2) | ||||||
FcγRIIIA | ||||||||||||
VV | 7 (12.7) | 10 (16.7) | .55 | 9 (15.8) | 5 (7.4) | .14 | 16 (14.3) | 15 (11.7) | .55 | |||
VF | 36 (65.5) | 21 (35) | .0035 | .0011 | 36 (63.1) | 33 (48.4) | .018 | .10 | 72 (64.3) | 54 (42.2) | .00028 | .00063 |
FF | 12 (21.8) | 29 (48.3) | .0030 | 12 (21.1) | 30 (44.1) | .0065 | 24 (21.4) | 59 (46.1) | .000061 | |||
FcγRIIIB | ||||||||||||
1/1 | 11 (19.3) | 8 (13.8) | 7 (11.9) | 10 (14.7) | 18 (15.5) | 18 (14.3) | ||||||
1/2 | 21 (36.9) | 23 (39.7) | .73 | 34 (57.6) | 35 (51.5) | .77 | 55 (47.4) | 58 (46.0) | .89 | |||
2/2 | 25 (43.8) | 27 (46.5) | 18 (30.5) | 23 (33.8) | 43 (37.1) | 50 (39.7) |
Genotype of variants of FcγRs, namely,FcγRIIA-131 H/R, FcγRIIIA158 V/F, and FcγRIIIB NA1/NA2, was determined for 2 cohorts of men who acquired HIV infection through sex with other men. In Population I (n = 119, KS = 58, and no KS = 61), an exploratory analysis was performed to test the hypothesis at each of 3 loci by χ2 analysis (3 × 2 tables with 2 degrees of freedom); no adjustments for multiple corrections are presented. Because the second cohort, Population II (n = 131, KS = 61, and no KS = 70), was tested to confirm the findings for Population I, a χ2 analysis (3 × 2 tables with 2 degrees of freedom) of the second population is presented without correction. The effect of each genotype for FcγRIIIA, namely, VV, VF, and FF on KS associated with HIV, is shown in a χ2 analysis (2 × 2 with one degree of freedom). The evidence for association in the combined population was investigated using the stratified analysis of Cochran-Mantel-Haenszel.49,50 There was no significant difference in χ2 analysis (3 × 2 tables with 2 degrees of freedom) of the 2 populations for distribution of genotype VV, VF, or FF overall, as well as for KS or no KS. There was no significant difference between no KS cohorts (ie, Population I, Population II, and the combined population) and normal healthy controls.32 Similarly, the distribution of genotypes ofFcγRIIA and FcγRIIIB was not significantly different overall from published, healthy control populations32 or when analyzed for the presence or absence of KS in the 2 populations.
Note: Not all samples could be amplified at each locus.