ABSTRACT
Genotyping of the hepatitis C virus (HCV) is crucial for determining the most efficient anti-viral therapy. The clinical sensitivity and specificity of the IntelliPlexTM HCV Genotyping Kit was determined by comparing the assay results of 307 specimens with the results obtained by Sanger sequencing. Out of 202 HCV-positive specimens tested, 8 samples yielded discrepant results between the IntelliPlex HCV Genotyping Kit and Sanger sequencing. For 5 of these discrepant samples, the IntelliPlex HCV Genotyping Kit classified the correct genotype but failed to show the same single or dual infected status as determined by Sanger sequencing. A total of 105 samples which tested negative for HCV by In-Vitro-Diagnostics (IVD)-approved viral load assay tested negative for HCV by the IntelliPlex HCV Genotyping Kit. The IntelliPlex HCV Genotyping Kit has a clinical specificity of 100% and a clinical sensitivity of 96.9% and is suited to be used in clinical laboratories to genotype HCV.
Subject(s)
Genotyping Techniques/standards , Hepacivirus/genetics , Hepatitis C/diagnosis , Reagent Kits, Diagnostic/standards , Genotype , Hepatitis C/virology , Humans , RNA, Viral/genetics , Sensitivity and Specificity , Viral LoadABSTRACT
Although the polymorphisms of PTPN22 and the variants of CTLA-4 have been reported to be the susceptibility genes, which increased risk of latent autoimmune diabetes in adults (LADA), the results remained inconclusive. The aim of this meta-analysis was to evaluate the association between the polymorphisms of two genes and LADA. We performed a systematic review by identifying relevant studies and applied meta-analysis to pool gene effects. Data from ten studies published between 2001 and 2013 were pooled for two polymorphisms: rs2476601 in the PTPN22 gene and rs231775 in the CTLA-4 gene. Data extraction and assessments for risk of bias were independently performed by two reviewers. Fixed-effect model and random-effect model were used to pool the odds ratios; meanwhile, heterogeneity test, publication bias and sensitive analysis were explored. The minor T allele at rs2476601 and the minor G at rs231775 carried estimated relative risks (odds ratio) of 1.52 (95 % CI 1.29-1.79) and 1.39 (95 % CI 1.11-1.74), respectively. These alleles contributed to an absolute lowering of the risk of all LADA by 4.88 and 14.93 % when individuals do not carry these alleles. The estimated lambdas were 0.49 and 0.63, suggesting a codominant model of effects was most likely for two genes. In summary, our systematic review has demonstrated that PTPN22 rs2476601 and CTLA-4 rs231775 are potential risk factors for LADA. An updated meta-analysis is required when more studies are published to increase the power of these polymorphisms and LADA.
