Sci Transl Med . SARS-CoV-2 infection drives an inflammatory response in human adipose tissue through infection of adipocytes and macrophages

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Sci Transl Med


. 2022 Sep 22;eabm9151.
doi: 10.1126/scitranslmed.abm9151. Online ahead of print.
SARS-CoV-2 infection drives an inflammatory response in human adipose tissue through infection of adipocytes and macrophages


Giovanny J Martínez-Colón ¹ , Kalani Ratnasiri ² , Heping Chen ¹ , Sizun Jiang ^{3 4} , Elizabeth Zanley ¹ , Arjun Rustagi ¹ , Renu Verma ¹ , Han Chen ³ , Jason R Andrews ¹ , Kirsten D Mertz ⁵ , Alexandar Tzankov ⁶ , Dan Azagury ⁷ , Jack Boyd ⁸ , Garry P Nolan ³ , Christian M Schürch ⁹ , Matthias S Matter ⁶ , Catherine A Blish ^{1 2 10} , Tracey L McLaughlin ¹



Affiliations

• PMID: 36137009
• DOI: 10.1126/scitranslmed.abm9151

Abstract

Obesity, characterized by chronic low-grade inflammation of the adipose tissue, is associated with adverse coronavirus disease 2019 (COVID-19) outcomes, yet the underlying mechanism is unknown. To explore whether severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection of adipose tissue contributes to pathogenesis, we evaluated COVID-19 autopsy cases and deeply profiled the response of adipose tissue to SARS-CoV-2 infection in vitro. In COVID-19 autopsy cases, we identified SARS-CoV-2 RNA in adipocytes with an associated inflammatory infiltrate. We identified two distinct cellular targets of infection: adipocytes and a subset of inflammatory adipose tissue-resident macrophages. Mature adipocytes were permissive to SARS-CoV-2 infection; although macrophages were abortively infected, SARS-CoV-2 initiated inflammatory responses within both the infected macrophages and bystander preadipocytes. These data suggest that SARS-CoV-2 infection of adipose tissue could contribute to COVID-19 severity through replication of virus within adipocytes and through induction of local and systemic inflammation driven by infection of adipose tissue-resident macrophages.