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SARS-CoV-2 exploits host DGAT and ADRP for efficient replication.

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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) exploits host lipid droplets for replication. Targeting diacylglycerol acyltransferase (DGAT) with xanthohumol inhibits viral spread and inflammation.

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Area of Science:

  • Virology
  • Metabolomics
  • Molecular Biology

Background:

  • Coronavirus Disease 2019 (COVID-19), caused by SARS-CoV-2, is a respiratory illness that profoundly alters host metabolism.
  • Metabolic dysregulation, particularly involving triacylglycerol (TG), is a hallmark of SARS-CoV-2 infection.

Purpose of the Study:

  • To investigate the role of host lipid metabolism in SARS-CoV-2 replication.
  • To identify host factors essential for viral propagation and explore therapeutic targets.

Main Methods:

  • Plasma lipidome analysis in COVID-19 patients.
  • Investigating the function of diacylglycerol acyltransferase (DGAT) and adipocyte differentiation-related protein (ADRP) in SARS-CoV-2 infection.
  • Utilizing DGAT gene depletion and a DGAT inhibitor (xanthohumol) in cellular and animal models.

Main Results:

  • Triacylglycerol (TG) is the dominant lipid class in SARS-CoV-2-induced metabolic changes.
  • Diacylglycerol acyltransferase (DGAT) and adipocyte differentiation-related protein (ADRP) are crucial host factors for SARS-CoV-2 replication.
  • SARS-CoV-2 nucleocapsid protein promotes lipid droplet (LD) formation via DGAT.
  • DGAT inhibition reduces viral protein synthesis and replication.
  • Xanthohumol suppresses SARS-CoV-2 replication and pulmonary inflammation in a hamster model.

Conclusions:

  • SARS-CoV-2 hijacks the host's lipid droplet machinery, specifically DGAT and ADRP, for efficient replication.
  • Targeting DGAT presents a promising therapeutic strategy for COVID-19 treatment, as demonstrated by xanthohumol's efficacy.