RAGE engagement by SARS-CoV-2 enables monocyte infection and underlies COVID-19 severity

Cell Rep Med. 2023 Nov 21;4(11):101266. doi: 10.1016/j.xcrm.2023.101266. Epub 2023 Nov 8.

Abstract

The spread of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has fueled the COVID-19 pandemic with its enduring medical and socioeconomic challenges because of subsequent waves and long-term consequences of great concern. Here, we chart the molecular basis of COVID-19 pathogenesis by analyzing patients' immune responses at single-cell resolution across disease course and severity. This approach confirms cell subpopulation-specific dysregulation in COVID-19 across disease course and severity and identifies a severity-associated activation of the receptor for advanced glycation endproducts (RAGE) pathway in monocytes. In vitro THP1-based experiments indicate that monocytes bind the SARS-CoV-2 S1-receptor binding domain (RBD) via RAGE, pointing to RAGE-Spike interaction enabling monocyte infection. Thus, our results demonstrate that RAGE is a functional receptor of SARS-CoV-2 contributing to COVID-19 severity.

Keywords: COVID-19; RAGE; SARS-CoV-2; disease severity; drug repurposing; longitudinal profiling; monocytes; single-cell multi-omics.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • COVID-19*
  • Humans
  • Monocytes
  • Pandemics
  • Receptor for Advanced Glycation End Products / genetics
  • SARS-CoV-2

Substances

  • Receptor for Advanced Glycation End Products
  • MOK protein, human