SARS-CoV-2 infects adipose tissue in a fat depot- and viral lineage-dependent manner.
Tatiana Dandolini SacconFelippe Mousovich-NetoRaissa Guimarães LudwigVictor Corasolla CarregariAna Beatriz Dos Anjos SouzaAmanda Stephane Cruz Dos PassosMatheus Cavalheiro MartiniPriscilla Paschoal BarbosaGabriela Fabiano de SouzaStefanie Primon MuraroJulia ForatoMariene Ribeiro AmorimRafael Elias MarquesFlavio Protasio VerasEster de A BarretoTiago Tomazini GonçalvesIsadora Marques PaivaNarayana P B FazoliniCarolina Mie Kawagosi OnoderaRonaldo Bragança Martins JuniorPaulo Henrique Cavalcanti de AraújoSabrina Setembre BatahRosa Maria Mendes VianaDanilo Machado de MeloAlexandre Todorovic FabroEurico ArrudaFernando Queiroz CunhaThiago Mattar CunhaMarco Antônio M PrettiBradley Joseph SmithHenrique Marques-SouzaThiago L KnittelGabriel Palermo RuizGerson S ProfetaTereza Cristina Minto Fontes-CalMariana BoroniMarco Aurélio Ramirez VinoloAlessandro S FariasPedro Manoel Mendes de Moraes-VieiraJoyce Maria Annichino BizzacchiTambet TeesaluFelipe David Mendonça ChaimEverton CazzoElinton Adami ChaimJosé Luis Proença ModenaDaniel Martins-de-SouzaMariana Kiomy OsakoLuiz Osório LeiriaMarcelo Alves da Silva MoriPublished in: Nature communications (2022)
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 counterparts. SARS-CoV-2 infection leads to inhibition of lipolysis in subcutaneous fat cells, while in visceral fat cells, it results in higher expression of pro-inflammatory cytokines. Viral load and cellular response are attenuated when visceral fat 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 fat cells, replicating and altering cell function and viability in a depot- and viral lineage-dependent fashion.