Overall survival of the patients with B-NHL and controls.

<p>Overall survival of the patients with B-NHL and controls.</p

Safety in the cohort treated by Peg-IFN-based therapy.

<p>Safety in the cohort treated by Peg-IFN-based therapy.</p

Flowchart.

<p>Peg-interferon-alpha (Peg-IFN), B-cell non-Hodgkin lymphoma (B-NHL) First generation of protease inhibitors (PI1s), Direct-acting antiviral drugs (DAAs).</p

Predictive factors associated with sustained virologic response in the cohort treated by Peg-IFN-based therapy.

<p>Predictive factors associated with sustained virologic response in the cohort treated by Peg-IFN-based therapy.</p

Sustained virologic response of the patients from the cohort treated by Peg-IFN-based therapy, * p< 0.02.

<p>First generation of protease inhibitors (PI1s). A: global sustained virologic response. B: sustained virologic response according to HCV genotype.</p

Characteristics and follow-up of the patients with HCV infection and B-NHL treated by direct-acting antiviral drugs (DAAs).

<p>Marginal zone lymphomas (MZLs); Diffuse large B-cell lymphomas (DLBCLs).</p

Characteristics of the patients treated by Peg-IFN-based therapy.

<p>Characteristics of the patients treated by Peg-IFN-based therapy.</p

Haematological response of the patients from the B-NHL group treated by Peg-IFN-based therapy with or without sustained virologic response, * p = 0.02.

<p>Haematological response of the patients from the B-NHL group treated by Peg-IFN-based therapy with or without sustained virologic response, * p = 0.02.</p

Combined Linkage and Association Studies Show that HLA Class II Variants Control Levels of Antibodies against Epstein-Barr Virus Antigens

<div><p>Over 95% of the adult population worldwide is infected with Epstein-Barr virus (EBV). EBV infection is associated with the development of several cancers, including Hodgkin lymphoma (HL). Elevated levels of anti-EBV antibodies have been associated with increased risk of HL. There is growing evidence that genetic factors control the levels of antibodies against EBV antigens. Here, we conducted linkage and association studies to search for genetic factors influencing either anti-viral capsid antigen (VCA) or anti-Epstein Barr nuclear antigen-1 (EBNA-1) IgG levels in a unique cohort of 424 individuals of European origin from 119 French families recruited through a Hodgkin lymphoma (HL) patient. No major locus controlling anti-VCA antibody levels was identified. However, we found that the HLA region influenced anti-EBNA-1 IgG titers. Refined association studies in this region identified a cluster of HLA class II variants associated with anti-EBNA-1 IgG titers (e.g. p = 5×10–5 for rs9268403). The major allele of rs9268403 conferring a predisposition to high anti-EBNA-1 antibody levels was also associated with an increased risk of HL (p = 0.02). In summary, this study shows that HLA class II variants influenced anti-EBNA-1 IgG titers in a European population. It further shows the role of the same variants in the risk of HL.</p></div

Genome-wide linkage analysis and association study of anti-EBNA-1 IgG levels in the linked 6p region.

<p>Top panel: Multipoint LOD score (left y-axis) and information content (right y-axis) are plotted along the 22 autosomes (x axis). Mid panel: Results of association study for 824 SNPs located in the 90% confidence linkage interval are given as −log₁₀ (pvalue) (y-axis) and plotted against SNP positions on chromosome 6 (x-axis in megabases). Bottom panel: Association results as −log₁₀ (pvalue) (y axis) with 1) the cluster of SNPs in strong linkage disequilibrium (r²>0.8) with rs9268403 (squares), and 2) the SNPs reported in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0102501#pone.0102501-Rubicz1" target="_blank">[3]</a>(circles); the two genotyped SNPs are shown under dominant model (plain symbol), and all the others SNPs are imputed and shown under additive model (open symbols); chromosome 6 position of SNPs and genes in the region are given on the x axis (in megabases).</p