Table 1.

Association between variant FcγRgenotypes and Kaposi's sarcoma (KS) in 2 populations of HIV-infected men

FcγR genotypes Population IPopulation 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 LocusGenotype 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 IPopulation 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 LocusGenotype 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.

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