Dataset Information

SARS-CoV-2 infects adipose tissue in a fat depot- and viral lineage-dependent manner

ABSTRACT: Visceral adiposity is a risk factor for severe COVID-19, and a link between adipose tissue infection and disease progression has been proposed. Here we demonstrate that SARS-CoV-2 infects human adipose tissue and undergoes productive infection in human primary adipose-derived stromal-vascular cells differentiated into adipocytes. However, the permissiveness to infection and the cellular response depends on the anatomical origin of the cells and the viral lineage. Cells of visceral adipose tissue origin express more ACE2 and are more permissive to SARS-CoV-2 infection than their subcutaneous counterpart. SARS-CoV-2 infection leads to inhibition of lipolysis in cells of subcutaneous origin, while in visceral fat cells, it results in higher expression of pro-inflammatory cytokines. Viral load and cellular response are attenuated when visceral adipose tissue cells are infected with the SARS-CoV-2 gamma variant. A similar degree of cell death occurs 4-days after SARS-CoV-2 infection, regardless of the cell origin or viral lineage. Hence, SARS-CoV-2 infects human adipose tissue cells, replicating and altering cell function and viability in a fat depot- and viral lineage-dependent fashion.

INSTRUMENT(S): Synapt MS

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Adipocyte, Mesenteric Adipose Tissue, Subcutaneous Adipose Tissue

DISEASE(S): Covid-19

SUBMITTER: Bradley Smith

LAB HEAD: Marcelo A. Mori

PROVIDER: PXD034510 | Pride | 2022-10-13

REPOSITORIES: Pride

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Publications

SARS-CoV-2 infects adipose tissue in a fat depot- and viral lineage-dependent manner.

Saccon Tatiana Dandolini TD Mousovich-Neto Felippe F Ludwig Raissa Guimarães RG Carregari Victor Corasolla VC Dos Anjos Souza Ana Beatriz AB Dos Passos Amanda Stephane Cruz ASC Martini Matheus Cavalheiro MC Barbosa Priscilla Paschoal PP de Souza Gabriela Fabiano GF Muraro Stéfanie Primon SP Forato Julia J Amorim Mariene Ribeiro MR Marques Rafael Elias RE Veras Flavio Protasio FP Barreto Ester E Gonçalves Tiago Tomazini TT Paiva Isadora Marques IM Fazolini Narayana P B NPB Onodera Carolina Mie Kawagosi CMK Martins Junior Ronaldo Bragança RB de Araújo Paulo Henrique Cavalcanti PHC Batah Sabrina Setembre SS Viana Rosa Maria Mendes RMM de Melo Danilo Machado DM Fabro Alexandre Todorovic AT Arruda Eurico E Queiroz Cunha Fernando F Cunha Thiago Mattar TM Pretti Marco Antônio M MAM Smith Bradley Joseph BJ Marques-Souza Henrique H Knittel Thiago L TL Ruiz Gabriel Palermo GP Profeta Gerson S GS Fontes-Cal Tereza Cristina Minto TCM Boroni Mariana M Vinolo Marco Aurélio Ramirez MAR Farias Alessandro S AS Moraes-Vieira Pedro Manoel M PMM Bizzacchi Joyce Maria Annichino JMA Teesalu Tambet T Chaim Felipe David Mendonça FDM Cazzo Everton E Chaim Elinton Adami EA Proença-Módena José Luiz JL Martins-de-Souza Daniel D Osako Mariana Kiomy MK Leiria Luiz Osório LO Mori Marcelo A MA

Nature communications 20220929 1

Visceral adiposity is a risk factor for severe COVID-19, and a link between adipose tissue infection and disease progression has been proposed. Here we demonstrate that SARS-CoV-2 infects human adipose tissue and undergoes productive infection in fat cells. However, susceptibility to infection and the cellular response depends on the anatomical origin of the cells and the viral lineage. Visceral fat cells express more ACE2 and are more susceptible to SARS-CoV-2 infection than their subcutaneous ...[more]

PMID: 36175400

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Project description:Background: Type I interferons (IFNs) are essential to the clearance of viral diseases, in part by initiating upregulation of IFN regulated genes (IRGs). A clear distinction between genes upregulated directly by virus and genes upregulated by secondary IFN production has not been made. Here we investigated the genes regulated by IFN-a2b compared to the genes regulated by SARS-CoV infection in ferrets. Methods: We characterized early host immune responses in peripheral blood and lung necropsies of ferrets injected with IFN-a2b or infected with SARS-CoV/Tor 2 strain, using microarray analysis on the Affymetrix platform. Results: We identified a common IRG signature that was upregulated in both SARS-CoV infected ferrets as well as in ferrets injected with IFN-a2b. We also identified unique patterns of gene expression for leukocyte activation, cell adhesion and complement pathways between IFN-a2b injection and SARS-CoV infection. Conclusions: Our results define the effects of IFN-a2b on the immune system of ferrets highlighting genes regulated by IFN during SARS-CoV infection. We have shown the similarities and differences of top funcional gene groups as well as pathways that play key roles in early immune responses in ferrets in response to IFN-a2b or SARS-CoV. Key words: ferret, gene expression, SARS, interferon. Keywords: time course In experiments with IFN-a2b, for peripheral blood, 15 ferrets were randomly allocated to 3 groups: Day 0, 5 ferrets (no IFN injection), day 1, 6 ferrets (injected), and day 2, 4 ferrets (injected). For lung necropsies of injected ferrets with IFN-a2b, we used 12 ferrets in 3 groups: 4 ferrets, day 0 (no IFN injection), 4 ferrets, day 1 (injected) and 4 ferrets, day 2 (injected). Experimental groups for SARS-CoV infection was as follows: For peripheral blood, 3 and 4 ferrets for day 0 (no infection) and day 2 (infection) respectively. For lung neceropsies, a total of 9 ferrets in 3 groups, each with 3 replicates for day 0 (no infection), day 1 (infection) and day 2 (infection).

Dataset Information

SARS-CoV-2 infects adipose tissue in a fat depot- and viral lineage-dependent manner

Publications

SARS-CoV-2 infects adipose tissue in a fat depot- and viral lineage-dependent manner.

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