Two novel HLA class II, HLA-DRB1*13:357 and HLA-DQB1*03:525, characterised in Russian individuals.
Two novel HLA class II, HLA-DRB1*13:357 and HLA-DQB1*03:525, characterised in Russian individuals.
The new HLA-DRB3*03:69 allele differs from DRB3*03:01:01:03 by change of C → G in exon 3.
HLA-A*24:630 differs from HLA-A*24:20:01:01 by one nucleotide substitution in codon 131 in exon 3.
A total of 43 novel HLA alleles detected in haematopoietic cell donors using single molecule real-time DNA sequencing.
The pathogenesis of COVID-19 warrants unravelling. Genetic polymorphism analysis may help answer the variability in disease outcome. To determine the role of KIR and HLA polymorphisms in susceptibility, progression, and severity of SARS-CoV-2 infection, 458 patients and 667 controls enrolled in this retrospective observational study from April to December 2020. Mild/moderate and severe/death study groups were established. HLA-A, -B, -C, and KIR genotyping were performed using the Lifecodes® HLA-SSO and KIR-SSO kits on the Luminex® 200™ xMAP fluoroanalyser. A probability score using multivariate binary logistic regression analysis was calculated to estimate the likelihood of severe COVID-19. ROC analysis was used to calculate the best cut-off point for predicting a worse clinical outcome with high sensitivity and specificity. A p ≤ 0.05 was considered statistically significant. KIR AA genotype protected positively against severity/death from COVID-19. Furthermore, KIR3DL1, KIR2DL3 and KIR2DS4 genes protected patients from severe forms of COVID-19. KIR Bx genotype, as well as KIR2DL2, KIR2DS2, KIR2DS3 and KIR3DS1 were identified as biomarkers of severe COVID-19. Our logistic regression model, which included clinical and KIR/HLA variables, categorised our cohort of patients as high/low risk for severe COVID-19 disease with high sensitivity and specificity (Se = 94.29%, 95% CI [80.84–99.30]; Sp = 84.55%, 95% CI [79.26–88.94]; OR = 47.58, 95%CI [11.73–193.12], p < 0.0001). These results illustrate an association between KIR/HLA ligand polymorphism and different COVID-19 outcomes and remarks the possibility of use them as a surrogate biomarkers to detect severe patients in possible future infectious outbreaks.
A missense nucleotide substitution at codon 95 of HLA-C*18:01:01:01 creates a novel allele HLA-C*18:20.
The coding sequence of HLA-B*40:540N differs from HLA-B*40:02:01:01 by a non-synonymous nucleotide substitution in exon 3.
HLA-A*24:617 differs from HLA-A*24:02:01:01 by one nucleotide in exon 4.
HLA-A*33:33:02 differs from HLA-A*33:33:01 by one synonymous nucleotide change C>T in exon 3 (TCC>TCT).
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