{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,4]],"date-time":"2026-11-04T20:00:55Z","timestamp":1793822455720,"version":"4.6.1"},"reference-count":265,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,6,22]],"date-time":"2026-06-22T00:00:00Z","timestamp":1782086400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>Viral pneumonia remains a preeminent global health threat, frequently culminating in acute respiratory distress syndrome (ARDS) and systemic organ failure. While traditional paradigms have centered on protein-based inflammatory cascades, this review synthesizes a vast body of emerging evidence to redefine viral pneumonia as a profound systemic metabolic crisis, specifically characterized by the radical remodeling of the host lipidome. Based on a meta-synthesis of clinical and mechanistic data, we delineate a consistent \u201cmetabolic crash\u201d during severe infection, where a precipitous decline in serum low-density lipoprotein (LDL)-cholesterol and the functional conversion of high-density lipoprotein (HDL) from a protective \u201cimmunometabolic shield\u201d into a pro-inflammatory vehicle serve as decisive prognostic indicators. We further dissect the molecular mechanisms of this reprogramming, detailing how respiratory viruses hijack the host SREBP-SCAP axis to repurpose lipid droplets for viral assembly, while simultaneously triggering ferroptotic cell death through the exhaustion of the GPX4-lipid-peroxidase defense system. By integrating the \u201cgut-lipid-lung axis\u201d and the role of systemic metainflammation, we illustrate how the host\u2019s baseline metabolic architecture dictates the threshold for lethal alveolar-capillary barrier failure. Finally, we evaluate the therapeutic potential of restoring lipid homeostasis through specialized pro-resolving mediators (SPMs) and metabolic stabilizers. We conclude that transitioning toward a lipid-centric precision medicine model, supported by AI-driven metabolic endotyping, is essential for advancing host-directed therapies in the management of severe respiratory viral infections.<\/jats:p>","DOI":"10.3389\/fimmu.2026.1836315","type":"journal-article","created":{"date-parts":[[2026,6,22]],"date-time":"2026-06-22T04:36:05Z","timestamp":1782102965000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["Serum lipidome remodeling in viral pneumonia: from pathophysiology to therapeutics"],"prefix":"10.3389","volume":"17","author":[{"given":"Yige","family":"Wang","sequence":"first","affiliation":[{"name":"Second Clinical Medical College, Nanjing Medical University","place":["Nanjing, Jiangsu, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qiang","family":"Xiao","sequence":"additional","affiliation":[{"name":"Department of Pulmonary and Critical 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