Frontiers in immunologyOct 29, 2026

Single-cell analysis reveals lasting changes in liver immune and metabolism cells after COVID-19 infection in obese individuals

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Updated Nov 2, 2026

Abstract

Obese mice exhibited persistent liver injury characterized by increased lipid accumulation and cellular apoptosis following SARS-CoV-2 infection.

Obesity is associated with ongoing inflammation and fibrosis in the lungs of infected mice.
Liver injury in obese mice includes metabolic dysfunction that persists beyond the acute phase of infection.
Single-cell RNA sequencing identified significant changes in immune and metabolic programs in the liver of obese mice post-infection.
Hepatic macrophages in obese mice showed lasting inflammatory and metabolic transcriptional changes.
Hepatocytes displayed altered functions related to glucose and fat metabolism.
Endothelial cells in the liver exhibited prolonged transcriptional changes linked to immune activation and clotting risk.

Simplified

SARS-CoV-2 infection affects multiple organs, and chronic post-viral tissue injury is often associated with persistent immune dysregulation. Obesity and related metabolic disorders are major risk factors for severe COVID-19 and post-acute sequelae of SARS-CoV-2 infection (PASC), including liver dysfunction. To define hepatic responses during post-acute infection, we studied lean and diet-induced obese mice at 7 and 28 days following infection with mouse-adapted SARS-CoV-2. Compared with lean mice, obese mice exhibited persistent lung inflammation and fibrosis, along with liver injury characterized by increased lipid accumulation, cellular apoptosis, and metabolic dysfunction. Single-cell RNA sequencing revealed obesity-associated alterations in hepatic immune and metabolic programs during post-acute infection. In particular, hepatic macrophages in obese mice showed sustained inflammatory and metabolic transcriptional alterations, while hepatocytes displayed altered programs associated with gluconeogenesis and lipid metabolism. Endothelial cells also exhibited persistent transcriptional changes linked to immune activation and prothrombotic pathways. These alterations remained evident at 28 days post-infection, suggesting incomplete restoration of immune and metabolic homeostasis in obese liver. Collectively, our findings reveal persistent obesity-associated hepatic immunometabolic remodeling following SARS-CoV-2 infection and identify cellular and molecular programs that may contribute to post-acute liver sequelae in metabolically compromised hosts.

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Single-cell analysis reveals lasting changes in liver immune and metabolism cells after COVID-19 infection in obese individuals

Abstract

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