Pairwise D' LD based on Cramer's V correlation coefficient between the presence and absence of different KIR genes in the two groups of patients (A: Non Sustained Viral Responders, NSVR; B: Sustained Viral Responders, SVR).

<p>In this approach to assessing KIR LD, the KIR cluster genetic polymorphism is considered simply as the presence (POS) or absence (NEG) of KIR genes. Note: Several conditions were applied for this analysis: 1) <i>KIR3DL3, KIR3DP1, KIR2DL4</i> and <i>KIR3DL2</i> were not included because they were present in all patients (framework genes), 2) <i>KIR2DL2</i> and <i>KIR2DL3</i> were considered as alleles of the same locus, 3) <i>KIR2DL5</i> was differentiated in <i>KIR2DL5A</i> and <i>KIR2DL5B</i> because they are located at different positions, and 4) <i>KIR2DS3</i> was included in the centromeric region.</p

KIR genotypes and haplotype frequencies of the studied population, and combinations of Cen and Tel haplotypes with HLA-B and HLA-C.

<p><b>Note</b>: ¹B/B and A/B genotypes were included in this group.</p><p>Tel-HLA-C, Cen-HLA-B and Cen-HLAB combinations were not significant.</p

Genotyping and frequencies of <i>KIR2DL2</i> and <i>KIR2DL3</i> alleles in relation to treatment outcome.

<p>Genotyping and frequencies of <i>KIR2DL2</i> and <i>KIR2DL3</i> alleles in relation to treatment outcome.</p

ROC curve of logic regression model using <i>IFNL3</i> C/C and KIR/HLA gene determination (<i>KIR2DL2/3</i>, <i>KIR2DL2/3-HLA</i> and KIR haplotype study) (solid line).

<p>We also included the ROC curves of <i>IFNL3</i> (dotted line) and <i>KIR2DL2/3-HLA</i> (dashed line) logic model determinations. It can be observed they do not overlap with the best logic regression model. Note: Area under the curve (AUC) of the best model: 0.729 (95% CI, 0.692–0.772).</p

Prediction of treatment outcome in patients with chronic HCV infection using the proposed logic regression model.

<p>Note:</p>1<p><i>IFNL3</i> polymorphism rs12979860.</p>2<p>KIR2DL2/3, KIR2DL2/3-HLA and KIR haplotype study.</p>3<p>Positive predictive value.</p>4<p>Negative predictive value.</p>5<p>Area under the curve.</p

KIR genotype distribution in the study cohort.

<p>The genotypes were deduced from KIR profiles as previously described <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0099426#pone.0099426-Pyo1" target="_blank">[10]</a>, <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0099426#pone.0099426-Hsu2" target="_blank">[33]</a>. Note: ¹ID assigned by the Allele Frequency Net Database (<a href="http://www.allelefrequencies.net" target="_blank">http://www.allelefrequencies.net</a>)</p

Note: Cen-AA (X1), Cen-BB (X2), IFNL3-G/G (X3), IFNL3-G/T (X4), IFNL3-T/T (X5), HOMOKIR2DL3-C1C1 (X6), HOMOKIR2DL2-C1C1 (X7), HOMOKIR2DL2-C1C2 (X8) viral load less than 400000 UI/ml (X9).

<p>Note: Cen-AA (X1), Cen-BB (X2), IFNL3-G/G (X3), IFNL3-G/T (X4), IFNL3-T/T (X5), HOMOKIR2DL3-C1C1 (X6), HOMOKIR2DL2-C1C1 (X7), HOMOKIR2DL2-C1C2 (X8) viral load less than 400000 UI/ml (X9).</p

KIR gene frequencies, <i>KIR2DL2/3-HLA</i> and <i>KIR2DS2-HLA</i> genotypes distribution in the two groups of patients.

<p>KIR gene frequencies, <i>KIR2DL2/3-HLA</i> and <i>KIR2DS2-HLA</i> genotypes distribution in the two groups of patients.</p