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10.1038/s41421-021-00338-2

http://scihub22266oqcxt.onion/10.1038/s41421-021-00338-2
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34702802!8548329!34702802
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suck abstract from ncbi


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pmid34702802      Cell+Discov 2021 ; 7 (1): 100
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  • SARS-CoV-2 exploits host DGAT and ADRP for efficient replication #MMPMID34702802
  • Yuan S; Yan B; Cao J; Ye ZW; Liang R; Tang K; Luo C; Cai J; Chu H; Chung TW; To KK; Hung IF; Jin DY; Chan JF; Yuen KY
  • Cell Discov 2021[Oct]; 7 (1): 100 PMID34702802show ga
  • Coronavirus Disease 2019 (COVID-19) is predominantly a respiratory tract infection that significantly rewires the host metabolism. Here, we monitored a cohort of COVID-19 patients' plasma lipidome over the disease course and identified triacylglycerol (TG) as the dominant lipid class present in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-induced metabolic dysregulation. In particular, we pinpointed the lipid droplet (LD)-formation enzyme diacylglycerol acyltransferase (DGAT) and the LD stabilizer adipocyte differentiation-related protein (ADRP) to be essential host factors for SARS-CoV-2 replication. Mechanistically, viral nucleo capsid protein drives DGAT1/2 gene expression to facilitate LD formation and associates with ADRP on the LD surface to complete the viral replication cycle. DGAT gene depletion reduces SARS-CoV-2 protein synthesis without compromising viral genome replication/transcription. Importantly, a cheap and orally available DGAT inhibitor, xanthohumol, was found to suppress SARS-CoV-2 replication and the associated pulmonary inflammation in a hamster model. Our findings not only uncovered the mechanistic role of SARS-CoV-2 nucleocapsid protein to exploit LDs-oriented network for heightened metabolic demand, but also the potential to target the LDs-synthetase DGAT and LDs-stabilizer ADRP for COVID-19 treatment.
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