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. 2019 Jan 24;10:53. doi: 10.3389/fimmu.2019.00053

Table 1.

Association of APOL1 G1-G2 variants with HIV-1 acquisition.

HIV-1 status n Age (years)$ Female& (%) No. G1-G2 risk alleles Comparison Model* OR (95% CI)* P*
0 1 2
Seroincident (SI) 227 39.9 ± 6.3 25.1 88 (38.8%) 110 (48.5%) 29 (12.8%) SI vs. SN Add 1.07 (0.84–1.38) 0.57
Addadj 1.07 (0.83–1.37) 0.61
Dom 1.13 (0.80–1.60) 0.47
Domadj 1.10 (0.78–1.57) 0.56
Rec 1.02 (0.62–1.70) 0.98
Recadj 1.04 (0.63–1.74) 0.87
Seroincident (SI) + seroprevalent (SP) 441 40.5 ± 6.2 25.0 177 (41.8%) 217 (49.2%) 47 (10.7%) SI+SP vs. SN Add 0.99 (0.80–1.23) 0.96
Addadj 1.00 (0.81–1.24) 0.99
Dom 1.07 (0.80–1.43) 0.64
Domadj 1.07 (0.80–1.43) 0.64
Rec 0.83 (0.54–1.30) 0.42
Recadj 0.84 (0.54–1.31) 0.45
Seronegative (SN) 335 41.5 ± 7.4 29.3 140 (41.8%) 153 (45.7%) 42 (12.5%) Reference - -

There were no associations between APOL1 kidney risk allele status and HIV-1-infection status. $P > 0.05 for SN vs. SI + SP; P < 0.05 for SN vs. SI; & P > 0.05 for SN vs. SI+SP or SN vs. SI.

*

Logistic regression for additive (Add, 2 vs. 1 vs. 0), dominant (Dom, 2 or 1 vs. 0), and recessive (Rec, 2 vs. 1 or 0) genetic models, adjusted (adj) for age (years) and stratified on sex.