iScienceOct 23, 2026

Long COVID is linked to changes in essential fatty acid breakdown by lipoxygenase

Updated Oct 24, 2026

Abstract

Plasma samples from 106 participants showed that upregulation of certain fatty acid metabolites during acute SARS-CoV-2 infection is associated with the later development of Long COVID.

Increased levels of polyunsaturated fatty acid metabolites linked to inflammation were observed in the acute phase of infection among those who later developed Long COVID.
Participants diagnosed with Long COVID exhibited changes in lipid metabolism compared to those who recovered over the months following infection.
Uncoupling of normal fatty acid metabolism was evident in Long COVID participants, indicating a potential alteration in inflammation resolution mechanisms.

Simplified

Long COVID (LC) represents a failure of healthy resolution mechanisms for inflammation after SARS-CoV-2 infection. Dietary essential polyunsaturated fatty acids (PUFAs) and their downstream metabolites can orchestrate inflammation resolution, suggesting these pathways may be altered in LC. In this study, plasma samples from two independent participant cohorts totaling 106 participants (designated by chart review as LC or Recovered) were collected longitudinally in the 12 months following SARS-CoV-2 infection and analyzed by mass spectrometry for targeted PUFA metabolites. In the acute phase of SARS-CoV-2 infection, upregulation of PUFA metabolites downstream of 12-lipoxygenase was associated with later development of LC. In the months following infection, LC participants displayed uncoupling of PUFA-related lipid metabolism and altered lipoxygenase-driven metabolism over time compared to recovered participants. These results provide new mechanistic insights for the development of LC and suggest potential therapeutic strategies for this prevalent and debilitating disorder.

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Long COVID is linked to changes in essential fatty acid breakdown by lipoxygenase

Abstract

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