1. SARS-CoV-2 infects adipose tissue in a fat depot- and viral lineage-dependent manner.
- Author
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Saccon TD, Mousovich-Neto F, Ludwig RG, Carregari VC, Dos Anjos Souza AB, Dos Passos ASC, Martini MC, Barbosa PP, de Souza GF, Muraro SP, Forato J, Amorim MR, Marques RE, Veras FP, Barreto E, Gonçalves TT, Paiva IM, Fazolini NPB, Onodera CMK, Martins Junior RB, de Araújo PHC, Batah SS, Viana RMM, de Melo DM, Fabro AT, Arruda E, Queiroz Cunha F, Cunha TM, Pretti MAM, Smith BJ, Marques-Souza H, Knittel TL, Ruiz GP, Profeta GS, Fontes-Cal TCM, Boroni M, Vinolo MAR, Farias AS, Moraes-Vieira PMM, Bizzacchi JMA, Teesalu T, Chaim FDM, Cazzo E, Chaim EA, Proença-Módena JL, Martins-de-Souza D, Osako MK, Leiria LO, and Mori MA
- Subjects
- Adipose Tissue, Angiotensin-Converting Enzyme 2, Cytokines, Humans, COVID-19, SARS-CoV-2
- 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 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., (© 2022. The Author(s).)
- Published
- 2022
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