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

Author:

Zhan Yan1234,Ye Ling5,Ouyang Qianying1234,Yin Jiye1234,Cui Jiajia6,Liu Ke1234,Guo Chengxian5,Zhang Haibo7,Zhai Jingbo8,Zheng Chunfu9ORCID,Guo Aoxiang1011,Sun Bao12

Affiliation:

1. Department of Clinical Pharmacology, Xiangya Hospital Central South University Changsha China

2. Hunan Key Laboratory of Pharmacogenetics, Institute of Clinical Pharmacology Central South University Changsha China

3. Engineering Research Center of Applied Technology of Pharmacogenomics Ministry of Education Beijing China

4. National Clinical Research Center for Geriatric Disorders Changsha China

5. Center of Clinical Pharmacology, The Third Xiangya Hospital Central South University Changsha China

6. Department of Geriatric Surgery, Xiangya Hospital Central South University Changsha China

7. Hangzhou Women's Hospital Hangzhou China

8. Key Laboratory of Zoonose Prevention and Control at Universities of Inner Mongolia Autonomous Region, Medical College Inner Mongolia Minzu University Tongliao China

9. Department of Microbiology, Immunology and Infectious Diseases, Cumming School of Medicine University of Calgary Calgary Alberta Canada

10. Department of Pharmacy, The Seventh Affiliated Hospital Sun Yat‐sen University Shenzhen China

11. Shenzhen Key Laboratory of Chinese Medicine Active substance screening and Translational Research Shenzhen China

12. Department of Pharmacy, The Second Xiangya Hospital Central South University Changsha China

Abstract

AbstractThe 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.

Publisher

Wiley

Subject

Infectious Diseases,Virology

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