Scientists discover why some people still can’t taste food after COVID-19 — SkimNews
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- Researchers from the University of Colorado Anschutz and two Swedish universities published a study in Chemical Senses examining 28 people whose taste disturbances persisted more than a year after COVID-19 — none had been hospitalized — marking the first direct biological evidence of measurable changes inside taste cells of long-COVID patients.
- Eleven of the 28 participants reported difficulty detecting sweet, bitter, and umami flavors specifically, while their sense of salty and sour remained largely intact; 8 of 28 had clearly abnormal taste scores on testing.
- Scientists identified reduced levels of mRNA producing PLCβ2, a protein that amplifies taste signals to the brain — the molecular defect specifically disrupts sweet, bitter, and umami detection because salty and sour use different signaling pathways that do not depend on PLCβ2.
- Thomas Finger, PhD, corresponding author and professor of cell and developmental biology at the University of Colorado Anschutz, described PLCβ2 as 'a molecular amplifier inside taste cells' whose reduction weakens the signal before it reaches the brain.
- Tissue microscopy also revealed structural disorganization in some participants' taste buds, suggesting both molecular signaling defects and physical architectural changes contribute to persistent taste dysfunction rather than a purely chemical problem.
- The durability puzzle: taste cells normally regenerate every two to four weeks, yet the molecular signaling disruptions appear to persist far longer in a subset of patients, potentially explaining why recovery can stretch beyond a year for this group.
- Open questions flagged by the authors: whether the PLCβ2 abnormalities can eventually normalize on their own, and whether restoring healthy taste signaling could serve as a treatment target for long-COVID taste loss.
Why it matters: For the small but real subset of long-COVID patients with taste loss persisting past a year, the study supplies the first measurable biological mechanism — not just self-reported symptoms — giving researchers a concrete molecular target (PLCβ2 restoration) to test for treatment. Clinicians previously had no biological anchor for this complaint; now the field can ask whether reversing the protein deficit actually recovers taste function.
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