Health
SARS-CoV-2 spike promotes metabolic rewiring of hepatocytes
Proteomic analysis revealed changes in hACE2 mouse hepatocytes after infection with pseudotyped viral particles expressing SARS-CoV-2 spikes. Volcano plot showing 354 differentially expressed peptides among hACE2 mouse hepatocytes in the presence (+) or absence (-) of pseudotyped virus particles after 48 h. b Volcano plot showing 132 differentially expressed peptides among WT mouse hepatocytes in the presence (+) or absence (−) of pseudotyped virus particles. See Supplementary Data 1 for a detailed list of all peptides with fold-changes and p-values. d Heatmap showing the top 25 upregulated or downregulated peptides among hACE2 mouse hepatocytes in the presence (+) or absence (−) of pseudotyped virus particles. eGene Ontology terms enhanced pathways representing unique differentially expressed peptides in WT (+ vs. -) or hACE2 (+ vs. -) mouse hepatocyte comparisons. The number of proteins belonging to the identified dysregulated pathways (left) and corresponding p-values (right) are shown. credit: communication biology (2022). DOI: 10.1038/s42003-022-03789-9
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes multiple organ damage, including liver dysfunction observed in more than 50% of COVID-19 patients. According to a study conducted at CIC bioGUNE, liver damage in patients with COVID-19 can be attributed to cytopathic effects induced by interactions between the virus and hepatocytes, increased immune responses, or drugs associated with the treatment of these patients. It may be due to toxicity.
Since the beginning of the pandemic, the effects of SARS-CoV-2 on the liver have been widely debated. “Clinical studies performed in patients with COVID-19 described liver lesions, but whether the observed damage was a direct result of SARS-CoV-2 tropism to this organ, or conversely, However, it was not clear whether it was a result of liver damage or the administration of the antibiotic/antiviral therapy used in these patients,” said María Mercado Gómez, first author of the publication. In this context, upper respiratory tractViruses such as SARS-CoV and MERS-CoV show liver tropism, so we wonder if the novel coronavirus can do that as well,” explains Dr. Prieto Fernández.
Dr. Martínez-Chantar and Dr. Asís Palazón’s group at CIC bioGUNE have synergized their expertise in the study of hepatocytes and immunology to demonstrate that hepatocytes are derived from a different model, humanized angiotensin-converting enzyme-2. We demonstrated that primary hepatocytes are susceptible to infection. (hACE2) mouse and primary human hepatocytes.This study was also the result of collaboration with the labs of Dr. Jiménez-Barbero, Dr. Nogueiras, Dr. Vicent Prevot, and Dr. Félix Elortza, and the results were communication biology17 August 2022.
“We used pseudotyped virus particles decorated with SARS-CoV-2 spike particles that induce the expression of ZsGreen in host cells upon infection, a fluorescent protein that allows quantification of infection by flow cytometry. is,” explains Dr. Prieto-Fernandez.
After demonstrating the interaction of the SARS-CoV-2 spike with hepatocytes, the researchers used a series of procedures to study the metabolic effects of this interaction. This includes metabolic flux experiments using carbon-labeled glucose and proteomic analysis by liquid chromatography tandem mass. Spectroscopic measurement. This multi-method approach led to the discovery that the SARS-CoV-2 spike not only accelerates the metabolic reprogramming of hepatocytes to glycolysis, but also impairs mitochondrial activity. my liver hurts Related to COVID-19.
“Importantly, we found that primary human hepatocytes and hACE2 hepatocytes in which steatosis and inflammation were induced by methionine and choline deficiency were more vulnerable to infection, and these data suggest that Supports metabolically related patient predispositions. fatty liver disease, MAFLD, make the prognosis of COVID-19 more severe,” said Dr. Malu Martinez-Chantar. Hepatocellular infection in humans and mice.
In summary, this study provides evidence that hepatocytes are susceptible to SARS-CoV-2 pseudovirus infection, making metformin a therapeutic option to mitigate SARS-CoV-2 infection in patients with fatty liver. I suggest that it is possible.
Maria Mercado-Gómez et al, SARS-CoV-2 spike promotes metabolic rewiring of hepatocytes, communication biology (2022). DOI: 10.1038/s42003-022-03789-9
Provided by CIC bioGUNE
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