SARS-CoV-2 infects human adipose tissue, with visceral fat cells being significantly more susceptible to infection and exhibiting a 240-fold higher viral load than subcutaneous fat cells.
SARS-CoV-2 productively infects human adipose tissue, with visceral fat showing greater susceptibility and pro-inflammatory response, potentially explaining the link between visceral adiposity and severe COVID-19.
Effect estimate: 240-fold higher
p-value: p=<0.0001
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.
Saccon et al. (Thu,) conducted a other in COVID-19 (n=47). SARS-CoV-2 infection in visceral adipose tissue cells vs. SARS-CoV-2 infection in subcutaneous adipose tissue cells was evaluated on Viral load at 24 hours post-infection (240-fold higher, p=<0.0001). SARS-CoV-2 infects human adipose tissue, with visceral fat cells being significantly more susceptible to infection and exhibiting a 240-fold higher viral load than subcutaneous fat cells.