ArticleFrontiers in immunology2026
SARS-CoV-2-infected adipocytes drive adipose inflammation and hepatocyte lipid accumulation.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Obesity and fatty liver may worsen COVID-19 outcomes, but the mechanism by which adipose tissue infection contributes to liver injury is unclear. We aimed to determine whether SARS-CoV-2 infection of human adipocytes promotes inflammation and hepatic lipid accumulation, and to identify the underlying mechanisms. Methods: Mesenchymal stem cell-derived human adipocytes were infected with Wuhan SARS-CoV-2 strain. Cell-surface ACE2 expression was measured in adipocytes. Viral replication and infectious titers were measured, and adipocyte morphology, cytokine/adipokine secretion, and lipid metabolism gene expression were analyzed. Culture supernatants from infected adipocytes were then applied to Huh7.5 hepatocytes to evaluate steatosis and fibrogenic activation. Results: SARS-CoV-2 productively infected adipocytes, which express cell-surface ACE2, leading to hypertrophy, increased IL-6 secretion, a higher leptin/adiponectin ratio, and lipid droplet accumulation. The infectious virus was released into the supernatants. However, neutralization with anti-Spike antibodies or UV-C inactivation abolished this effect, indicating that hepatocyte lipid accumulation depended on infectious virus rather than on soluble adipocyte-derived mediators alone. Discussion: Adipose tissue can serve as a source of infectious SARS-CoV-2 that promotes hepatic steatosis and fibrogenic activation, suggesting a mechanism by which obesity and fatty liver may worsen COVID-19 outcomes, although the contribution of residual infectious virus versus adipocyte-derived factors cannot be fully distinguished. At present, the data do not support an independent role for adipocyte-derived soluble mediators in this effect. The study is intended as a mechanistic
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