ArticleFrontiers in immunology2026
Divergent lipid utilization strategies of SARS-CoV-2 and MERS-CoV revealed by comparative multi-omics profiling of infected mouse lung tissues.
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
Background: Coronaviruses (CoVs), including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and Middle East respiratory syndrome (MERS-CoV), cause respiratory infections with distinct clinical outcomes and case fatality rates. However, the molecular basis of these differences remains unclear. In this study, we sought to define virus-specific host metabolic programs by directly comparing multiomics profiles of the lungs of lethally infected mouse models. Methods: We performed integrated multiomics analyses, including untargeted metabolomics, transcriptomics, and targeted lipidomics, of lung tissues from human angiotensin-converting enzyme 2 (hiACE2)-human dipeptidyl peptidase 4 (hDPP4) double-knock-in (DKI) mice infected in SARS-CoV-2 or MERS-CoV. Data Integration Analysis and Biomarker discovery using Latent cOmponents (DIABLO) was applied across all three omics layers to identify key distinguishing molecular patterns. Additionally, Results: We identified two distinct strategies for lipid utilization. SARS-CoV-2 infection showed strong activation of energy and amino acid metabolism at an early stage of infection (3 days post infection, DPI), whereas MERS-CoV infection was characterized by sustained alterations in lipid and nucleotide metabolism. Integrative DIABLO analysis of all three omics layers revealed that the key distinguishing features clustered into virus-specific molecular signatures: a triacylglycerol-lipid droplet-interferon axis for SARS-CoV-2 and a phospholipid-sphingolipid-membrane hub for MERS-CoV. Conclusion: These findings show that β-CoVs exploit host lipid metabolism through virus-specific and time-dependent remodeling programs, providing a framework for understanding differential pathogenesis and developing host-directed antiviral strategies.
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