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The ORF8 protein of SARS-CoV-2 mediates immune evasion through down-regulating MHC-Ι

Yiwen Zhang1, Yingshi Chen1, Yuzhuang Li1

  • 1Institute of Human Virology, Key Laboratory of Tropical Disease Control of Ministry of Education, Guangdong Engineering Research Center for Antimicrobial Agent and Immunotechnology, Zhongshan School of Medicine, Sun Yat-sen University, 510080, Guangzhou, Guangdong, China.

Proceedings of the National Academy of Sciences of the United States of America
|May 22, 2021
PubMed

Insights

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection down-regulates major histocompatibility complex class I (MHC-I) via its ORF8 protein. This viral mechanism helps SARS-CoV-2 evade immune detection by cytotoxic T lymphocytes.

Area of Science:

  • Immunology
  • Virology
  • Molecular Biology

Background:

  • COVID-19, caused by SARS-CoV-2, presents distinct clinical features compared to SARS.
  • Understanding SARS-CoV-2 immune evasion mechanisms is crucial for combating the pandemic.

Purpose of the Study:

  • To investigate how SARS-CoV-2 evades cellular immune surveillance.
  • To identify specific viral components involved in immune evasion.

Main Methods:

  • In vitro and in vivo studies of SARS-CoV-2 infected cells.
  • Analysis of major histocompatibility complex class I (MHC-I) expression.
  • Investigation of the role of SARS-CoV-2 ORF8 protein.

Main Results:

  • SARS-CoV-2 infection down-regulates MHC-I expression in infected cells.
  • The viral ORF8 protein directly interacts with MHC-I, leading to its degradation via autophagy.
  • ORF8-expressing cells show reduced sensitivity to cytotoxic T lymphocyte lysis due to impaired antigen presentation.

Conclusions:

  • SARS-CoV-2 utilizes its ORF8 protein to down-regulate MHC-I, thereby evading cytotoxic T lymphocyte surveillance.
  • Targeting ORF8 could be a potential therapeutic strategy to enhance immune responses against SARS-CoV-2.
Keywords:
MHC-ΙORF8SARS-CoV-2immune evasion

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