KIR gene profiles in our study populations.

<p>A total of 42 KIR gene profiles were identified (panel A). Genotype ID number reported are those from the reference database [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0117420#pone.0117420.ref028" target="_blank">28</a>]. The presence of KIR genes is indicated by grey shanding. Genotypes AA and BX according to criteria reported in material and method section are indicated in the first column.°Only ID Genotypes present in at least two patients were reported in tables. Distribution of genotype ID1 and ID4 for HCV-negative patients and for patients with HCV infection and different outcomes (panel B). Distribution of KIR3DL1, KIR2DL3, KIR2DS4, KIR2DS3 genes ID4 for HCV-negative patients and for patients with HCV infection and different outcomes (panel C). * Fisher’s Exact test, p<0.05.</p

Distribution of KIR3DL1 gene and combination with HLA-B for patients with different HCV related disease outcomes.

<p>It is showed a negative trend association between the KIR3DL1/HLA-Bw4 with the presence of HCV-related lymphoma.</p

Cent/Tel KIR gene profiles in HCV-negative patients and patients with HCV infection and different outcomes.

<p>Distribution of Cent2 and Cent6 locus (panel A, <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0117420#pone.0117420.t002" target="_blank">Table 2</a>). Distribution of Tel3 and Tel6 loci (panel B, <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0117420#pone.0117420.t002" target="_blank">Table 2</a>). Distribution of Cent/Tel1 loci (panel C, <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0117420#pone.0117420.t002" target="_blank">Table 2</a>). Distribution of Cent/Tel1 with A/B KIR2DL5 variant (panel D, <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0117420#pone.0117420.t003" target="_blank">Table 3</a>). Distribution of Cent-2DS3/5 (1) loci (panel E, <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0117420#pone.0117420.t003" target="_blank">Table 3</a>). Distribution of Tel-2DS4 (3) AND Tel-2DS4 (8) locus (panel F, <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0117420#pone.0117420.t003" target="_blank">Table 3</a>). * Fisherx’s Exact test, p<0.05.</p

Centromeric and telomeric halves of KIR genotypes (panel A).

<p>A stretch of 14 kb DNA that interconnects KIR3DP1 and KIR2DL4 divides the KIR genotype into two halves. The centromeric half is delimited by 3DL3 and 3DP1, while the telomeric half is delimited by 2DL4 and 3DL2. There is different KIR gene content, due to a recombination of these genes, in KIR genotypes across individuals and populations. The framework genes, present in all genotypes are shown in grey boxes; genes encoding activating KIR are in red color; and those for inhibitory receptors are in blue color. KIR2DL4 encodes a receptor that has both inhibitory and activating functions The KIR2DP1 and 3DP1 (green) are pseudogenes that do not express a receptor. <b>Pairwise D’ LD based on Cramer’s V correlation coefficient between the presence and absence of different KIR genes in four groups of patients (panel B-E)</b> B: HCV negative; C: Chronic HCV; D: Hepatocellular carcinoma; E: Lymphoproliferative disease. The KIR cluster genetic polymorphism is considered as the presence or absence of KIR genes.</p