ArticleTranslational psychiatry2026
Fatigue after COVID-19 infection is associated with peripheral immunometabolic alterations affecting neuroimmune responses in the hippocampus.
Article in Translational psychiatry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fatigue is a common and disabling symptom reported following SARS-CoV-2 infection, yet the underlying biological mechanisms remain poorly understood. In this study, we investigated whether fatigue severity in individuals previously infected with SARS-CoV-2 is associated with immune and metabolic alterations in serum and whether these peripheral changes can influence hippocampal cell function in vitro. Serum cytokines, kynurenine pathway, and tryptophan-derived and monoamine-related metabolites were measured in a total of 38 individuals with past COVID-19 infection. Human hippocampal progenitor cells were exposed to 1% patient serum during proliferation and differentiation, with readouts including cytokine release, metabolite production, and markers of neurogenesis (doublecortin, DCX) and astrocytic reactivity (glial fibrillary acidic protein, GFAP; aquaporin-4, AQP4). Results show that fatigue severity correlates with lower serum levels of interleukin-8 (IL-8) and with lower levels of metabolites of the kynurenine pathway and tryptophan-derived and monoamine-related metabolites, including kynurenine (KYN) and quinolinic acid (QUIN), and 5-hydroxyindoleacetic acid (5HIAA). Exposure of hippocampal cells to serum from individuals with higher fatigue was associated with increased endogenous production of interleukin-13 (IL-13) and the kynurenine metabolite anthranilic acid (ANA) in the cell supernatant, as well as with increased neurogenesis (increased DCX expression) and enhanced astrocytic reactivity (increased GFAP expression). Notably, serum IL-8 level was inversely correlated with both cellular outcomes. Likewise, serum 5-HIAA levels were negatively correlated with IL-13 release, with mediation analysis indicating that 5-HIAA significantly mediated the association between fatigue severity and IL-13 production (71% explained). Overall, our results suggest that fatigue after COVID-19 infection is associated with neuroimmune and metabolic changes in hippocampal cells, involving peripheral serotonin metabolism (5-HIAA) and cytokine signalling (IL-13).
Indexed as
Identifiers
42457661What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.