Distribution of <scp>HLA</scp> allele frequencies in 82 Chinese individuals with coronavirus disease‐2019 (COVID‐19)

Wang, Wei; Zhang, Wei; Zhang, Jingjing; He, Ji; Zhu, Faming

doi:10.1111/tan.13941

Cited by 166 publications

(192 citation statements)

References 19 publications

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“…Wang et al have studied HLA allele frequencies in Chinese Han individuals with COVID‐19. An association between HLA allele distribution in COVID‐19 patients and healthy individuals was assessed 9 . In this study, 82 patients with COVID‐19 were genotyped for HLA‐A, ‐B, ‐C, ‐DRB1, ‐DRB3/4/5, ‐DQA1, ‐DQB1, ‐DPA1, and ‐DPB1 loci using next‐generation sequencing.…”

Section: Discussionmentioning

confidence: 99%

“…This study reported that frequencies of the HLA‐C*07:29 and HLA‐B*15:27 alleles were higher in COVID‐19 patients than those in the control population. Two different studies from Wang et al 9 and the severe COVID‐19 GWAS group were conducted in different countries, which might have led to different results 5 …”

Section: Discussionmentioning

confidence: 99%

“…In disease caused by SARS‐CoV in 2003, increased severity among individuals with HLA‐B*46:01 has been shown 8 . In addition, studies have demonstrated a possible association between HLA gene polymorphisms and susceptibility to SARS‐CoV 4,9 . Recently, Nguyen et al 7 have reported that HLA‐B*46:01 as the HLA allele with the fewest predicted binding peptides for SARS‐CoV‐2 as well as SARS‐CoV.…”

Section: Introductionmentioning

confidence: 99%

“…Recently, Nguyen et al 7 have reported that HLA‐B*46:01 as the HLA allele with the fewest predicted binding peptides for SARS‐CoV‐2 as well as SARS‐CoV. These results suggest that pairing HLA typing with COVID‐19 testing could improve assessment of the severity of the disease caused by SARS‐CoV‐2 7,9 . However, the association between HLA gene polymorphisms and risk for COVID‐19 has not been fully elucidated 1‐3,5,7 .…”

Section: Introductionmentioning

confidence: 99%

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Association between HLA gene polymorphisms and mortality of COVID‐19: An in silico analysis

Tomita

Ikeda

Sato

et al. 2020

Immunity Inflam & Disease

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Introduction The emergence of SARS‐CoV‐2 has caused global public health and economic crisis. Human leukocyte antigen (HLA) is a critical component of the viral antigen presentation pathway and plays essential roles in conferring differential viral susceptibility and severity of diseases. However, the association between HLA gene polymorphisms and risk for COVID‐19 has not been fully elucidated. We hypothesized that HLA genotypes might impact on the differences in morbidity and mortality of COVID‐19 across countries. Methods We conducted in silico analyses and examined an association of HLA gene polymorphisms with prevalence and mortality of COVID‐19 by using publicly available databases. Results We found that a possible association between HLA‐A*02:01 and an increased risk for COVID‐19. HLA‐A*02:01 had a relatively lower capacity to present SARS‐CoV‐2 antigens compared with other frequent HLA class I molecules, HLA‐A*11:01 or HLA‐A*24:02. Conclusion This study suggests that individuals with HLA‐A*11:01 or HLA‐A*24:02 genotypes may generate efficiently T‐cell‐mediated antiviral responses to SARS‐CoV‐2 compared with HLA‐A*02:01. The differences in HLA genotypes may potentially alter the course of the disease and its transmission.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Association between HLA gene polymorphisms and mortality of COVID‐19: An in silico analysis

Tomita

Ikeda

Sato

et al. 2020

Immunity Inflam & Disease

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“… 37 , 38 Furthermore, HLA polymorphic variation has been suggested to underlie the large variability in virus clearance that has been observed among individuals. 39 Our analysis of the largest antigen of SARS-CoV-2, S1 spike glycoprotein, suggests that aminopeptidase trimming can be a significant filter that helps shape which peptides will be presented by HLA. Thus, we propose a short list of candidate peptides that could be prioritized in downstream antigenic analysis as well as in vaccine design and efficacy studies ( Tables 1 and 2 ).…”

Section: Resultsmentioning

confidence: 92%

Generation of SARS-CoV-2 S1 Spike Glycoprotein Putative Antigenic Epitopes in Vitro by Intracellular Aminopeptidases

et al. 2020

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Presentation of antigenic peptides by MHCI is central to cellular immune responses against viral pathogens. While adaptive immune responses versus SARS-CoV-2 can be of critical importance to both recovery and vaccine efficacy, how protein antigens from this pathogen are processed to generate antigenic peptides is largely unknown. Here, we analyzed the proteolytic processing of overlapping precursor peptides spanning the entire sequence of the S1 spike glycoprotein of SARS-CoV-2, by three key enzymes that generate antigenic peptides, aminopeptidases ERAP1, ERAP2, and IRAP. All enzymes generated shorter peptides with sequences suitable for binding onto HLA alleles, but with distinct specificity fingerprints. ERAP1 was the most efficient in generating peptides 8–11 residues long, the optimal length for HLA binding, while IRAP was the least efficient. The combination of ERAP1 with ERAP2 greatly limited the variability of peptide sequences produced. Less than 7% of computationally predicted epitopes were found to be produced experimentally, suggesting that aminopeptidase processing may constitute a significant filter to epitope presentation. These experimentally generated putative epitopes could be prioritized for SARS-CoV-2 immunogenicity studies and vaccine design. We furthermore propose that this in vitro trimming approach could constitute a general filtering method to enhance the prediction robustness for viral antigenic epitopes.

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Genetics of COVID‐19 and myalgic encephalomyelitis/chronic fatigue syndrome: a systematic review

Tziastoudi

Cholevas

Stefanidis

et al. 2022

Ann Clin Transl Neurol

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COVID‐19 and ME/CFS present with some similar symptoms, especially physical and mental fatigue. In order to understand the basis of these similarities and the possibility of underlying common genetic components, we performed a systematic review of all published genetic association and cohort studies regarding COVID‐19 and ME/CFS and extracted the genes along with the genetic variants investigated. We then performed gene ontology and pathway analysis of those genes that gave significant results in the individual studies to yield functional annotations of the studied genes using protein analysis through evolutionary relationships (PANTHER) VERSION 17.0 software. Finally, we identified the common genetic components of these two conditions. Seventy‐one studies for COVID‐19 and 26 studies for ME/CFS were included in the systematic review in which the expression of 97 genes for COVID‐19 and 429 genes for ME/CFS were significantly affected. We found that ACE, HLA‐A, HLA‐C, HLA‐DQA1, HLA‐DRB1, and TYK2 are the common genes that gave significant results. The findings of the pathway analysis highlight the contribution of inflammation mediated by chemokine and cytokine signaling pathways, and the T cell activation and Toll receptor signaling pathways. Protein class analysis revealed the contribution of defense/immunity proteins, as well as protein‐modifying enzymes. Our results suggest that the pathogenesis of both syndromes could involve some immune dysfunction.

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Distribution of HLA allele frequencies in 82 Chinese individuals with coronavirus disease‐2019 (COVID‐19)

Cited by 166 publications

References 19 publications

Association between HLA gene polymorphisms and mortality of COVID‐19: An in silico analysis

Association between HLA gene polymorphisms and mortality of COVID‐19: An in silico analysis

Generation of SARS-CoV-2 S1 Spike Glycoprotein Putative Antigenic Epitopes in Vitro by Intracellular Aminopeptidases

Genetics of COVID‐19 and myalgic encephalomyelitis/chronic fatigue syndrome: a systematic review

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