CD14 Rs2569190 Research Articles

Association between the CD226 rs763361 polymorphism and susceptibility to autoimmune diseases: a meta-analysis

The aim of this study was to explore whether the CD226 rs763361 polymorphism confers susceptibility to autoimmune diseases. A meta-analysis was conducted on the associations between the CD226 rs763361 polymorphism and autoimmune diseases using: 1) allele contrast, and 2) the recessive, 3) dominant and 4) additive models. Ten articles that included 17 comparative studies on a total of 8900 patients and 10,295 controls were included in the meta-analysis. These studies were performed on seven European, five Asian and five South American sample populations. Meta-analysis of all study subjects revealed an association between the CD226 rs763361 T allele and the susceptibility to autoimmune diseases (odds ratio; OR 1.162, 95% confidence interval; CI 1.097-1.230, p < 1.0 × 10(-8)). Stratification by ethnicity indicated an association between the CD226 rs763361 T allele and autoimmune disease in Europeans and South Americans (OR 1.134, 95% CI 1.079-1.191, p = 6.7 × 10(-7); OR 1.308, 95% CI 1.160-1.475, p = 1.1 × 10(-5)) and between the CD226 rs763361 TT genotype and autoimmune disease in Asians (OR 1.366, 95% CI 1.130-1.650, p = 0.001). Disease-specific meta-analysis showed an association between systemic lupus erythematosus (SLE) and the CD226 rs763361 T allele (OR 1.150, 95% CI 1.040-1.271, p = 0.006), but no association between rheumatoid arthritis and the CD226 rs763361 polymorphism (OR for the T allele 1.207, 95% CI 0.913-1.596, p = 0.187). On the other hand, associations were found between the CD226 rs763361 T allele and systemic sclerosis (SSc) and type 1 diabetes (T1D) (OR 1.126, 95% CI 1.020-1.244, p = 0.019; OR 1.353, 95% CI 1.102-1.660, p = 0.004). This meta-analysis demonstrates the CD226 rs763361 polymorphism confers susceptibility to autoimmune disease in Europeans, South Americans and Asians, and in particular, shows that the CD226 rs763361 polymorphism is associated with SLE, SSc and T1D. These results support the existence of an association between the CD226 gene and a subgroup of autoimmune diseases.

Innate immunity gene single nucleotide polymorphisms and otitis media

ObjectiveToll-like receptors (TLR) activate the innate immune system. Single nucleotide polymorphisms (SNPs) in TLR genes are linked to increased susceptibility to infections. TLR4-deficient mice have increased incidence and duration of otitis media. We hypothesize that SNPs in TLR genes are more common in otitis-prone children than in children without a history of otitis media. MethodsCases (n=70) included children undergoing surgery for otitis media. Control subjects (n=70) included children undergoing surgery for non-otologic indication. Genomic DNA was extracted from blood samples. RT-PCR genotyping was performed for TLR2 (rs5743708), TLR4 (rs4986790 and rs4986791), TLR9 (rs5743836 & rs187084), and CD14 (rs2569190). ResultsThere were no significant differences between the groups in family history, day care, smoke exposure, allergies or prevalence of the SNPs. The most common pre-op diagnosis in control subjects was obstructive sleep apnea (OSA). ConclusionsTLR2, TLR4, TLR9 and CD14 gene SNPs were not more prevalent in otitis-prone children.

Gene–Gene Interactions between Candidate Gene Polymorphisms Are Associated with Total IgE Levels in Korean Children with Asthma

Objective. To investigate associations between total serum immunoglobulin E (IgE) levels and single nucleotide polymorphisms (SNPs) from eight candidate genes (IL-4 rs2243250, IL-4Rα rs1805010, IL-13 rs20541, IL-13Rα1 rs2495636, CD14 rs2569190, tumor necrosis factor-alpha (TNF-α) rs1800629, cytotoxic T lymphocyte-associated antigen (CTLA4) rs231775, FCER1B rs1441585) in children with asthma and to evaluate gene–gene interactions. Methods. A total of 669 Korean children with asthma (n = 544 atopic n = 125 non-atopic) were included. Asthma phenotypes, total serum IgE levels, and methacholine challenge test results were evaluated. SNPs were genotyped using the polymerase chain reaction-restriction fragment length polymorphisms (PCR-RFLP) method. Multi-factor dimensionality reduction (MDR) was used to analyze gene–gene interactions. Results. The combination of the IL-13, IL-13Rα1, and CTLA4 polymorphisms was selected through MDR analysis of the data pertaining to children with atopic and non-atopic asthma (accuracy = 0.5459, cross validation consistency (CVC) = 10/10). The IL-4Rα, IL-13, IL-13Rα1, CD14, and CTLA4 polymorphisms were selected as the best model of increased total serum IgE levels in non-atopic and atopic asthma (asthma: accuracy = 0.4726, CVC = 10/10; atopic asthma: accuracy = 0.4573, CVC = 10/10). Both the IL-4Rα and the IL-13 polymorphisms were correlated with the IgE level. ANOVA analysis revealed that the combinations of the CTLA4 and IL-13, IL-13 and IL-13Rα1, IL-4Rα and IL-13, and CD14 and IL-13 polymorphisms were all significantly associated with increased total serum IgE levels. Conclusions. The best model of increased IgE level included the IL-4Rα, IL-13, IL-13Rα1, CD14, and CTLA4 polymorphisms. Of the various interactions between these polymorphisms, the combinations of the CTLA4 and IL-13 polymorphisms and the IL-13 and IL-13Rα1 polymorphisms showed synergistic effects in terms of increased total serum IgE levels in the present cohort.

Influence of MIF, CD40, and CD226 polymorphisms on risk of rheumatoid arthritis

Macrophage migration inhibitory factor (MIF) is a key pro-inflammatory mediator. It plays an important role part in the pathogenesis of several inflammatory and immune diseases. A functional single nucleotide polymorphism (SNP) of MIF -173 G/C is known to influence MIF promoter activity in T lymphoblast cell lines and is associated with a higher serum MIF level. The CD40 is also crucial for some relevant functions of the immune system and may be related to rheumatoid arthritis (RA). And CD226 is an important cell-surface receptor molecule involved in the adhesion and activation of T-cell. We hypothesized that these polymorphisms may contribute to RA susceptibility. We studied MIF -173 G/C, CD40, and CD226 gene polymorphisms in 214 patients with RA and 478 controls in a Chinese population. Genotyping was done by using matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS). When the MIF -173 GG homozygote genotype was used as the reference group, the CC genotype was associated with a significantly increased risk for RA. In the recessive model, when the MIF -173 GG/GC genotypes were used as the reference group, the CC homozygote genotype was associated with a significant 1.56-fold increased susceptibility to RA. None of the CD40 rs1883832 C/T and CD226 rs763361 C/T polymorphisms achieved a significant difference in genotype distributions between cases and controls. In the stratification analyzes, a significantly increased risk for RA associated with the MIF -173 CC genotype was evident among CRP-negative patients compared with the MIF -173 GG/GC genotype. For the CD40 rs1883832 C/T variant, the risk effects of CD40 rs1883832 TT versus CD40 rs1883832 CC/CT were significant in men. These findings suggested that the functional SNP MIF -173 G/C variant allele was associated with the development of RA. However, CD40 and CD226 gene polymorphisms may not be associated with RA susceptibility. Due to the limitation of sample size, this study should be considered preliminary.

LADA and T1D in Estonian population — Two different genetic risk profiles

Aims/hypothesisThe aim of our study was to analyze combined impact of 17 polymorphisms at 8 gene regions previously shown to be associated with autoimmunity in diabetes. We hypothesized that the genetic predisposition is multiplicative and joint risk of different diabetic phenotypes forms by distinct combination of susceptibility loci. MethodsAn ethnically homogenous population of Estonian origin, including 65 LADA patients, 154 patients with T1D, 260 patients with T2D and 229 non-diabetic controls, was genotyped for polymorphisms/haplotypes in HLA-DQB1, insulin gene (rs689, rs3842729), PHTF1–PTPN22 region (rs2476601, rs6679677), CTLA4 region (rs231806, rs16840252, rs5742909, rs231775, rs3087243, rs2033171), ICOS region (rs10932037, rs4675379), CD25 (rs706778), CD226(rs763361), NAA25 (rs17696736). ResultsAs expected, the risk of T1D was consistently attributed by HLA-DQB1 haplotypes, but also by haplotypes of INS and PHTF1–PTPN22 region, and rs17696736 in NAA25. By contrast, LADA was associated only with T1D-protective HLA haplotypes and with two more frequent haplotypes of the CTLA4. It is of interest, that seldom CT haplotype of PHTF1–PTPN22 region carried the risk for autoantibody-negative T2D. The final best-fitted model for T1D genetic risk contained six gene regions (HLA-DQB1, INS, PHTF1, CTLA4 +49, CD226 and NAA25) and for LADA only two (HLA-DQB1 and CTLA4 +49). The AUCs of these models are 0.869 and 0.693, respectively. ConclusionsClassical T1D-risk haplotypes of HLA and some non-HLA loci describe quite well the genetic risk for T1D but not for LADA. The need of further studies should be stressed to discover the real risk factors for slower forms of autoimmune diabetes in adults.

A multicenter study confirms CD226gene association with systemic sclerosis-related pulmonary fibrosis

IntroductionCD226 genetic variants have been associated with a number of autoimmune diseases and recently with systemic sclerosis (SSc). The aim of this study was to test the influence of CD226 loci in SSc susceptibility, clinical phenotypes and autoantibody status in a large multicenter European population.MethodsA total of seven European populations of Caucasian ancestry were included, comprising 2,131 patients with SSc and 3,966 healthy controls. Three CD226 single nucleotide polymorphisms (SNPs), rs763361, rs3479968 and rs727088, were genotyped using Taqman 5'allelic discrimination assays.ResultsPooled analyses showed no evidence of association of the three SNPs, neither with the global disease nor with the analyzed subphenotypes. However, haplotype block analysis revealed a significant association for the TCG haplotype (SNP order: rs763361, rs34794968, rs727088) with lung fibrosis positive patients (PBonf = 3.18E-02 OR 1.27 (1.05 to 1.54)).ConclusionOur data suggest that the tested genetic variants do not individually influence SSc susceptibility but a CD226 three-variant haplotype is related with genetic predisposition to SSc-related pulmonary fibrosis.

Analysis of the association between CD40 and CD40 ligand polymorphisms and systemic sclerosis

IntroductionThe aim of the present study was to investigate the possible role of CD40 and CD40 ligand (CD40LG) genes in the susceptibility and phenotype expression of systemic sclerosis (SSc).MethodsIn total, 2,670 SSc patients and 3,245 healthy individuals from four European populations (Spain, Germany, The Netherlands, and Italy) were included in the study. Five single-nucleotide polymorphisms (SNPs) of CD40 (rs1883832, rs4810485, rs1535045) and CD40LG (rs3092952, rs3092920) were genotyped by using a predesigned TaqMan allele-discrimination assay technology. Meta-analysis was assessed to determine whether an association exists between the genetic variants and SSc or its main clinical subtypes.ResultsNo evidence of association between CD40 and CD40LG genes variants and susceptibility to SSc was observed. Similarly, no significant statistical differences were observed when SSc patients were stratified by the clinical subtypes, the serologic features, and pulmonary fibrosis.ConclusionsOur results do not suggest an important role of CD40 and CD40LG gene polymorphisms in the susceptibility to or clinical expression of SSc.

Opposite effects of allergy prevention depending on CD14 rs2569190 genotype in 3 intervention studies

Opposite effects of allergy prevention depending on CD14 rs2569190 genotype in 3 intervention studies

Abstract A64: Effects of genetic polymorphisms of innate immunity genes on the noncardia gastric cancer risk

Abstract Background and Objective: Increasing evidence suggests that polymorphisms in innate immunity genes are associated with Helicobacter pylori (H. pylori)-induced inflammation and may influence susceptibility to developing noncardia gastric cancer. Therefore, we investigated the effect of polymorphisms of TLR2, TLR4, and CD14, their combination and interaction with environmental factors on the noncardia gastric cancer risk in a Korean population. Methods: We genotyped four polymorphisms in three genes (TLR2, rs1898830 A&amp;gt;G; TLR4, rs10759932 T&amp;gt;C, rs10983755 A&amp;gt;G; CD14, rs2569190 T&amp;gt;C) in a case-control study of 487 noncardia gastric cancer patients and 487 sex- and age-matched healthy controls. Multiple logistic regression models were used to detect the effects of genetic polymorphisms and environmental factors, which was stratified by the histological type of gastric cancer. Results: TLR4 rs10983755 variant allele carriers were found to have a higher risk of intestinal type gastric cancer than homozygous wild-type carriers (OR [95% CI] = 1.40 [1.01–1.96], P = 0.046). Other genetic variants did not show any association with noncardia gastric cancer risk. When we examined the combined effect with other polymorphisms, the increased risk of intestinal type gastric cancer among TLR4 rs10983755 variant allele carriers compared to wild-type homozygous carriers were observed only among homozygous wild-type carriers of TLR2 rs1898830 (OR [95% CI] = 1.97 [1.24–3.12], P = 0.004) or CD14 rs2569190 (OR [95% CI] = 1.95 [1.31–2.91], P = 0.001). In addition, the effect of TLR4 rs10983755 variant allele on intestinal type gastric cancer was stronger among H. pylori-positive participants who are under 55 years old, smoke tobacco and drink alcoholic beverages. Conclusion: These results suggest that the genetic polymorphisms of these innate immunity genes are associated with the development of H. pylori-associated noncardia gastric cancer. Citation Information: Cancer Prev Res 2011;4(10 Suppl):A64.

A common SNP in the CD40 region is associated with systemic lupus erythematosus and correlates with altered CD40 expression: implications for the pathogenesis

BackgroundIn systemic lupus erythematosus (SLE) sustained CD40L expression by T cells and platelets activates a variety of cells via its receptor CD40 contributing to disease pathogenesis. Although CD40 has recently...

A CD40 and an NCOA5 gene polymorphism confer susceptibility to psoriasis in a Southern European population: A case–control study

Recent genome-wide association studies of many complex diseases have successfully identified novel susceptibility loci, with many of them shared by multiple disease-associated pathways. The genes CD40 and nuclear receptor coactivator 5 ( NCOA5), located in a 400-kb region surrounding CD40, have been reported to be associated with increased risk for rheumatoid arthritis and other autoimmune diseases. We hypothesized that those genes may also have a role in psoriasis (PS), an autoimmune, chronic inflammatory skin disease. In a case–control study, 198 patients with PS and 400 controls were genotyped for 2 single nucleotide polymorphisms (SNPs) of the CD40 and NCOA5 genes located on chromosome 20q.12–q13.12. Here, we demonstrate for the first time the association of both SNPs with susceptibility to PS, thus suggesting a putative key role of both genes in multiple autoimmune diseases. Alleles G and C of the CD40 rs4810485 and NCOA5 rs2903908 SNPs, respectively, were more common in individuals with PS than in controls ( p = 0.03, odds ratio [OR] = 1.42, 95% confidence interval [95% CI] 1.05–1.95 and p = 0.000 003, OR = 1.93, 95% CI 1.47–2.55, respectively). The identification of shared genetic susceptibility loci may provide insight into our understanding of the pathophysiology of autoimmune diseases.

Association of the CD226 Ser307 variant with systemic sclerosis: Evidence of a contribution of costimulation pathways in systemic sclerosis pathogenesis

The nonsynonymous polymorphism rs763361 of the CD226 gene, which encodes DNAX accessory molecule 1, which is involved in T cell costimulation pathways, has recently been identified as a genetic risk factor for autoimmunity. The purpose of this study was to test for association of the CD226 rs763361 polymorphism with systemic sclerosis (SSc) in European Caucasian populations. CD226 rs763361 was genotyped in 3,632 individuals, consisting of a discovery sample (991 SSc patients and 1,008 controls) and a replication sample (999 SSc patients and 634 controls). All study subjects were of European Caucasian origin. Expression of CD226 was assessed on peripheral blood mononuclear cells obtained from 21 healthy donors genotyped for CD226 rs763361. The CD226 rs763361 T allele was found to be associated with SSc in both the discovery and the replication samples, showing the following results in the combined populations: odds ratio (OR) 1.22 (95% confidence interval [95% CI] 1.10-1.34), P = 5.69 × 10(-5) . The CD226 T allele was also associated with various SSc subsets, highlighting a potential contribution to disease severity. The most remarkable associations of the CD226 TT risk genotype were observed with the diffuse cutaneous SSc subtype, the anti-topoisomerase I antibody-positive, and SSc-related fibrosing alveolitis subsets: OR 1.86 (95% CI 1.42-2.43), P = 5.15 × 10(-6) , OR 1.82 (95% CI 1.38-2.40), P = 2.16 × 10(-5) , and OR 1.61 (95% CI 1.25-2.08), P = 2.73 × 10(-4) , respectively. CD226 expression was not significantly influenced by CD226 rs763361 genotypes whatever the T cell subtype investigated. Our results establish CD226 as a new SSc genetic susceptibility factor underlying the contribution of costimulation pathways in the pathogenesis of SSc. Further work is nevertheless needed to define the causal variant at the CD226 locus as well as the functional consequences.

Genetic association and functional consequences of a common SNP in the CD40 region with systemic lupus erythematosus and rheumatoid arthritis in a homogeneous Greek population

BackgroundThere is increasing evidence that different autoimmune diseases may share some common pathogenetic pathways. The CD40 locus has recently been identified by a genome-wide study as a genetic risk factor...

Evaluation of the established non-MHC multiple sclerosis loci in an Indian population

Background: Multiple sclerosis (MS) is a chronic demyelinating neurodegenerative disorder with a strong genetic component. Objective: The prevalence of MS in India is low compared with white populations of Northern European descent. Methods: In order to ascertain whether disease susceptibility genes are the same across different populations, we completed the first investigation in the Indian MS population of 15 MS loci outside of the major histocompatibility (MHC) region that were previously identified and validated with MS susceptibility through genome-wide association and replication studies in white populations. Results: In total, 197 Indian patients and 197 unrelated controls were analyzed. The most associated single nucleotide polymorphism (SNP) within this study was rs6897932 in the IL7R gene, which showed a strong protective effect in this data set (rs 6897932, OR = 0.5543, 95% CI = 0.37–0.78, p = 0.0009727). Two other SNPs were nominally associated with MS in this dataset, namely CLEC16A rs 12708716 (p = 0.0082, OR = 1.478, 95% CI = 1.106–1.975) and CD226 rs763361 (p = 0.03971, OR = 1.353, CI = 1.014–1.805). For the majority of the remaining SNPs (7/14), the trend for association was in the same direction as in previous studies in the white population. Conclusions: Although the power of this study was limited, our preliminary data suggest that disease susceptibility genes in MS in the Indian population may be similar to those of western populations.

Influence ofCD40rs1883832 Polymorphism in Susceptibility to and Clinical Manifestations of Biopsy-proven Giant Cell Arteritis

To assess the potential association between CD40 rs1883832 polymorphism and biopsy-proven giant cell arteritis (GCA). We also studied the influence of the polymorphism on phenotypic expression of this vasculitis, in particular the development of visual ischemic manifestations. Three hundred five Spanish patients with biopsy-proven GCA and 788 matched controls were assessed. DNA from patients and controls was obtained from peripheral blood. Samples were genotyped for the CD40 rs1883832 C/T polymorphism using a predesigned TaqMan allele discrimination assay and by polymerase chain reaction amplification. Patients with GCA showed a trend toward a higher frequency of the minor allele homozygote of rs1883832 (TT) compared to healthy controls (12.1% vs 8.3%, respectively; p = 0.05, OR 1.54, 95% CI 0.98-2.40). Also, a marginally significant increased frequency of the minor allele T was observed in patients with GCA who had visual ischemic manifestations (36.9%) compared to those without visual ischemic manifestations (27.7%; p = 0.04, OR 1.53, 95% CI 0.99-2.34). In this regard, patients with GCA carrying the minor allele T (either TT or TC) experienced visual ischemic manifestations more commonly than those carrying the CC genotype (58.5% vs 44.2%; p = 0.04, OR 1.78, 95% CI 0.99-3.22). Our results suggest a potential implication of the CD40 rs1883832 C/T polymorphism in susceptibility to visual ischemic manifestations in individuals with biopsy-proven GCA.

CD40: Novel Association with Crohn's Disease and Replication in Multiple Sclerosis Susceptibility

BackgroundA functional polymorphism located at −1 from the start codon of the CD40 gene, rs1883832, was previously reported to disrupt a Kozak sequence essential for translation. It has been consistently associated with Graves' disease risk in populations of different ethnicity and genetic proxies of this variant evaluated in genome-wide association studies have shown evidence of an effect in rheumatoid arthritis and multiple sclerosis (MS) susceptibility. However, the protective allele associated with Graves' disease or rheumatoid arthritis has shown a risk role in MS, an effect that we aimed to replicate in the present work. We hypothesized that this functional polymorphism might also show an association with other complex autoimmune condition such as inflammatory bowel disease, given the CD40 overexpression previously observed in Crohn's disease (CD) lesions.MethodologyGenotyping of rs1883832C>T was performed in 1564 MS, 1102 CD and 969 ulcerative colitis (UC) Spanish patients and in 2948 ethnically matched controls by TaqMan chemistry.Principal FindingsThe observed effect of the minor allele rs1883832T was replicated in our independent Spanish MS cohort [p = 0.025; OR (95% CI) = 1.12 (1.01–1.23)]. The frequency of the minor allele was also significantly higher in CD patients than in controls [p = 0.002; OR (95% CI) = 1.19 (1.06–1.33)]. This increased predisposition was not detected in UC patients [p = 0.5; OR (95% CI) = 1.04 (0.93–1.17)].ConclusionThe impact of CD40 rs1883832 on MS and CD risk points to a common signaling shared by these autoimmune conditions.

The role of lipopolysaccharide in the development of atopy in humans

Atopy is a highly prevalent condition and remains the single biggest risk factor for asthma. Although atopy has a heritable component, the time frame of the increase in the prevalence indicates that it is not due to genetic factors alone. The relationship between allergen exposure and sensitization is complex. Lipopolysaccharide (LPS) and its bioactive moiety endotoxin are common to all gram-negative bacteria, and have been used as a surrogate of microbial load. Endotoxin can be readily measured in dust collected from homes. Some studies have demonstrated a clear inverse dose-response relationship between exposure to endotoxin and the risk of atopy but this finding has not been reproduced in all studies. Our innate immune system recognizes LPS readily via the LPS signal transduction pathway, which has the trimolecular complex of CD14/TLR4/MD2 at the core. A common single-nucleotide polymorphism in the promoter region of CD14 rs2569190 C to T (CD14/-260 or CD14/-159) has been associated with elevated sCD14. Although early studies suggested that this variant was associated with more severe atopy, this finding was not uniformly replicated. It has now been demonstrated in four independent populations that high exposure to endotoxin in the domestic environment is protective against the development of atopy, but only among carriers of the C allele, that is, the environmental exposure is only relevant when taken in the context of the genotype. Furthermore, this interaction is biologically plausible. We propose that neither the environmental exposure nor the genotype in isolation is sufficient to cause complex diseases like asthma and atopy, but disease results from the one acting in the context of the other, of which CD14 and endotoxin is one example contributing to the risk for atopy.

Lack of an Association between CD14 Gene Variants and Disease Manifestations in Chronic Hepatitis C

Objective: Progressive hepatic fibrosis and cirrhosis develops in patients with chronic liver diseases irrespectively of etiology and with a marked inter-individual variability. Gut-derived bacterial lipopolysaccharides (endotoxin) have been shown to act as cofactors exacerbating ongoing liver disease. The T allele of a single nucleotide polymorphism (SNP), rs2569190 / C-159T, in the endotoxin receptor CD14 gene has been reported to be related to susceptibility to ethanol-induced liver cirrhosis. Our study aimed at analyzing the association of this SNP with disease progression in chronic hepatitis C. Materials and Methods: Liver biopsy specimens from a total of 137 patients with chronic hepatitis C virus (HCV) infection were evaluated regarding necroinflammatory activity (grading), architectural changes (staging), and further histological lesions characteristic for hepatitis C. HCV types, epidemiological data, and biochemical parameters were monitored in parallel. Samples of genomic DNA were genotyped at the respective position by 5rsquor;-nuclease assays using fluorescent dye-labelled allele-specific probes. Results: Genotype distribution of 30: 70: 37 (CC: CT: TT) was close to that given for Caucasians in public data bases and followed Hardy-Weinberg equilibrium (p=0.8645). Patients homozygous for the T allele were significantly younger than patients with other genotypes. However, CD14 rs2569190 / C-159T genotype was neither found to be associated with fibrosis, inflammatory activity, other histological manifestations typical for hepatitis C, HCV types, sex nor with biochemical data. Conclusion: Our data thus failed to reveal any association of CD14 rs2569190 / C-159T with clinical parameters of chronic HCV infection as it was observed by other groups (1,2).