On the peptide binding affinity changes in population-specific HLA repertoires to the SARS-CoV-2 variants Delta and Omicron

Chen, Lu-Chun; Nersisyan, Stepan; Wu, Chang-Jiun; Chang, Che‐Mai; Tonevitsky, Alexander G.; Guo, Chin-Lin; Chang, Wei Chiao

doi:10.1016/j.jaut.2022.102952

Cited by 7 publications

(13 citation statements)

References 33 publications

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“…Reduced vaccine efficacy and increased disease susceptibility are other phenotypes of SARS‐CoV‐2 immune evasion. Chen et al investigated the S protein‐HLA binding affinity profiles of the Wuhan strain and two dominant variants (Delta and Omicron) in Taiwanese, British, and Russian populations 49 and found that in the Delta strain, the tight binding of the viral S protein to HLA was reduced in all three populations. In contrast, the reduction in the Omicron strain was more pronounced in Taiwanese.…”

Section: Discussionmentioning

confidence: 99%

The binding profile of SARS‐CoV‐2 with human leukocyte antigen polymorphisms reveals critical alleles involved in immune evasion

Zhan,

Ye,

Ouyang

et al. 2023

Journal of Medical Virology

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The COVID‐19 pandemic, caused by the severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2), astonished the world and led to millions of deaths. Due to viral new mutations and immune evasion, SARS‐CoV‐2 ranked first in transmission and influence. The binding affinity of human leukocyte antigen (HLA) polymorphisms to SARS‐CoV‐2 might be related to immune escape, but the mechanisms remained unclear. In this study, we obtained the binding affinity of SARS‐CoV‐2 strains with different HLA proteins and identified 31 risk alleles. Subsequent structural predictions identified 10 active binding sites in these HLA proteins that may promote immune evasion. Particularly, we also found that the weak binding ability with HLA class I polymorphisms could contribute to the immune evasion of Omicron. These findings suggest important implications for preventing the immune evasion of SARS‐CoV‐2 and providing new insights for the vaccine design.

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Section: Discussionmentioning

confidence: 99%

The binding profile of SARS‐CoV‐2 with human leukocyte antigen polymorphisms reveals critical alleles involved in immune evasion

Zhan,

Ye,

Ouyang

et al. 2023

Journal of Medical Virology

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“…87 Given the highly mutagenic profile that SARS-CoV-2 has, 93 in addition to the characteristic variability of HLA, 94 infection with new viral variants may induce non-recognition by the binding grooves present in the proteins of the complex, this being an activity linked to loss of peptide affinity that results in a delayed immune response (Figure 3). 95,96 Alterations in peptide affinity in the MHC, specifically for HLA, have been previously reported in several pathologies and associated with the progression of the pathological picture. 96 Recent studies have evaluated the antigen-HLA relationship in the Delta and Omicron variants, and it was possible to conclude that there is a great loss of recognition affinity for HLA proteins, 93 where class II is impaired and does not promote in a timely manner the differentiation of TCD4+ cells, therefore, an immune escape.…”

Section: Hla-mediated Immune Response To Sars-cov-2mentioning

confidence: 99%

“…96 Recent studies have evaluated the antigen-HLA relationship in the Delta and Omicron variants, and it was possible to conclude that there is a great loss of recognition affinity for HLA proteins, 93 where class II is impaired and does not promote in a timely manner the differentiation of TCD4+ cells, therefore, an immune escape. 95,96…”

Section: Hla-mediated Immune Response To Sars-cov-2mentioning

confidence: 99%

“…Given the highly mutagenic profile that SARS-CoV-2 has, 93 in addition to the characteristic variability of HLA, 94 infection with new viral variants may induce non-recognition by the binding grooves present in the proteins of the complex, this being an activity linked to loss of peptide affinity that results in a delayed immune response (Figure 3). 95,96…”

Section: Introductionmentioning

confidence: 99%

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Influence of polymorphic variations of IFNL, HLA, and IL-6 genes in severe cases of COVID-19

Araújo,

Sgorlon,

Aguiar

et al. 2023

Exp Biol Med (Maywood)

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The administration of vaccination doses to the global population has led to a decrease in the incidence of COVID-19. However, the clinical picture developed by infected individuals remains extremely concerning due to the great variability in the severity of cases even in vaccinated individuals. The clinical progression of the pathology is characterized by various influential factors such as sex, age group, comorbidities, and the genetics of the individual. The immune response to viral infections can be strongly influenced by the genetics of individuals; nucleotide variations called single-nucleotide polymorphisms (SNPs) in structures involved in the innate and adaptive immune response such as interferon (IFN)-λ, human leukocyte antigen (HLA), and interleukin (IL)-6 are frequently associated with pathological progression. In this study, we conducted a review of the main SNPs of these structures that are associated with severity in COVID-19. Searches were conducted on some platforms of the National Center for Biotechnology and Information (NCBI), and 102 studies were selected for full reading according to the inclusion criteria. IFNs showed a strong association with antiviral function, specifically, IFN-λ3 (IL-28B) demonstrated genetic variants commonly related to clinical progression in various pathologies. For COVID-19, rs12979860 and rs1298275 presented frequently described unfavorable genotypes for pathological conditions of hepatitis C and hepatocellular carcinoma. The high genetic variability of HLA was reported in the studies as a crucial factor relevant to the late immune response, mainly due to its ability to recognize antigens, with the HLA-B*46:01 SNP being associated with susceptibility to COVID-19. For IL-6, rs1554606 showed a strong relationship with the clinical progression of COVID-19. In addition, rs2069837 was identified with possible host protection relationships when linked to this infection.

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“…Just as the binding affinity of EBV peptides to MHC class II molecules can influence the generation of an antiviral response [ 191 , 218 ], it could also occur with SARS-CoV-2 [ 388 ]. It is known that single amino acid alterations in immunogenic peptides can enhance or decrease the binding of the peptide to the MHC class II molecule, causing the differentiation of CD4 T cells into Th1 cells if the binding is strong or into Th2 cells if the binding is weak [ 389 ].…”

Section: Role Of Ebv In Me/cfs and Long Covidmentioning

confidence: 99%

Epstein–Barr virus-acquired immunodeficiency in myalgic encephalomyelitis—Is it present in long COVID?

Ruiz-Pablos,

Paiva,

Zabaleta

2023

J Transl Med

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Both myalgic encephalomyelitis or chronic fatigue syndrome (ME/CFS) and long COVID (LC) are characterized by similar immunological alterations, persistence of chronic viral infection, autoimmunity, chronic inflammatory state, viral reactivation, hypocortisolism, and microclot formation. They also present with similar symptoms such as asthenia, exercise intolerance, sleep disorders, cognitive dysfunction, and neurological and gastrointestinal complaints. In addition, both pathologies present Epstein–Barr virus (EBV) reactivation, indicating the possibility of this virus being the link between both pathologies. Therefore, we propose that latency and recurrent EBV reactivation could generate an acquired immunodeficiency syndrome in three steps: first, an acquired EBV immunodeficiency develops in individuals with “weak” EBV HLA-II haplotypes, which prevents the control of latency I cells. Second, ectopic lymphoid structures with EBV latency form in different tissues (including the CNS), promoting inflammatory responses and further impairment of cell-mediated immunity. Finally, immune exhaustion occurs due to chronic exposure to viral antigens, with consolidation of the disease. In the case of LC, prior to the first step, there is the possibility of previous SARS-CoV-2 infection in individuals with “weak” HLA-II haplotypes against this virus and/or EBV.

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On the peptide binding affinity changes in population-specific HLA repertoires to the SARS-CoV-2 variants Delta and Omicron

Cited by 7 publications

References 33 publications

The binding profile of SARS‐CoV‐2 with human leukocyte antigen polymorphisms reveals critical alleles involved in immune evasion

The binding profile of SARS‐CoV‐2 with human leukocyte antigen polymorphisms reveals critical alleles involved in immune evasion

Influence of polymorphic variations of IFNL, HLA, and IL-6 genes in severe cases of COVID-19

Epstein–Barr virus-acquired immunodeficiency in myalgic encephalomyelitis—Is it present in long COVID?

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