SARS-CoV-2 Infection Alters the Phenotype and Gene Expression of Adipocytes

Abstract

Epidemiological evidence emphasizes that excess fat mass is associated with an increased risk of severe COVID-19 disease. Nevertheless, the intricate interplay between SARS-CoV-2 and adipocytes remains poorly understood. It is crucial to decipher the progression of COVID-19 both in the acute phase and on long-term outcomes. In this study, an in vitro model using the human SGBS cell line (Simpson-Golabi-Behmel syndrome) was developed to investigate the infectivity of SARS-CoV-2 in adipocytes, and the effects of virus exposure on adipocyte function. Our results show that SGBS adipocytes expressing ACE2 are susceptible to SARS-CoV-2 infection, as evidenced by the release of the viral genome into the medium, detection of the nucleocapsid in cell lysates, and positive immunostaining for the spike protein. Infected adipocytes show remarkable changes compared to uninfected controls: increased surface area of lipid droplets, upregulated expression of genes of inflammation (Haptoglobin, MCP-1, IL-6, PAI-1), increased oxidative stress (MnSOD), and a concomitant reduction of transcripts related to adipocyte function (leptin, fatty acid synthase, perilipin). Moreover, exogenous expression of spike protein in SGBS adipocytes also led to an increase in lipid droplet size. In conclusion using the human SGBS cell line, we detected SARS-CoV-2 infectivity in adipocytes, revealing substantial morphological and functional changes in infected cells.

FABP4 as a Therapeutic Host Target Controlling SARS-CoV2 Infection

“…40 showing that cells transfected with virus non-structural proteins (nsp 3,4 and 6) to form RO-like structures (ROLS) also accumulate, then consume LDs during the process of ROLS formation. A recent study reported an increase in the LD area of infected Simpson-Golabi-Behmel syndrome (SGB)-derived adipocytes 42 . This might be a result of the timepoint in which this analysis was made in addition to variations in dynamics of cellular responses to infection across the hTERT and SGB-derived adipocytes.…”