Summary: For a small subset of “long COVID” patients, the world has remained flavorless for over a year. A new study inally provides the “smoking gun” for this condition.
By performing biopsies on human taste buds, scientists identified a specific molecular defect: a drastic reduction in PLCβ2 mRNA. This protein acts as a signal amplifier for sweet, bitter, and umami flavors. Without it, the “volume” of taste signals is turned down so low the brain can’t detect them, even though the virus itself is long gone.
Key Facts
- The “Amplifier” Defect: Researchers found reduced levels of PLCβ2, a critical protein that strengthens signals inside taste cells before they are sent to the brain.
- Selective Taste Loss: The defect specifically affects sweet, bitter, and umami receptors. Salty and sour tastes remain largely intact because they use different signaling pathways that don’t rely on PLCβ2.
- Structural Disorganization: Beyond molecular changes, microscopic exams revealed that some patients’ taste buds were physically disorganized, further disrupting the sensory map.
- Persistent Signaling Failure: While taste cells typically regenerate every 2–4 weeks, the study proves that in some patients, the cellular “instruction manual” for these new cells remains corrupted for over a year.
- Direct Biological Evidence: This is the first study to link subjective patient reports of long-term taste loss to measurable, quantitative biological abnormalities in the taste buds.
Source: University of Colorado
Scientists have identified molecular and structural changes in taste buds that may explain why a small subset of people experience long-term taste loss after COVID-19 infection.
The study, published last month in Chemical Senses, provides the first direct evidence linking patients’ reported taste changes to measurable biological abnormalities inside taste cells.
What causes long-term taste loss after COVID-19?
Researchers from the University of Colorado Anschutz and two Swedish universities studied 28 non-hospitalized patients who reported persistent taste disturbances more than one year after contracting COVID-19.
Key findings:
- 8 of 28 patients showed clearly abnormal taste test scores
- 11 patients reported specific loss of sweet, bitter and umami taste
- Salty and sour taste were largely preserved
To understand why, researchers performed biopsies on taste buds from 20 participants.
Molecular defect identified in taste receptor cells
The team, organized by Göran Hellekant, PhD, of the University of Wisconsin and the Swedish University Of Agricultural Sciences, discovered reduced levels of messenger RNA (mRNA) responsible for producing a protein called PLCβ2 — a critical signal amplifier in receptor cells that detect sweet, bitter and umami tastes.
“PLCβ2 acts like a molecular amplifier inside taste cells,” said Thomas Finger, PhD, professor of cell and developmental biology at the University of Colorado Anschutz and corresponding author of the study. “It strengthens the signal before it’s transmitted to the brain. When levels are reduced, the taste signal weakens.”
Importantly, taste cells that detect salty and sour flavors do not rely on this protein, which may explain why those tastes are less affected.
Structural changes also observed
In addition to molecular abnormalities, some patients showed altered taste bud organization under microscopic examination.
“Some subjects had normal-looking taste buds, while others showed structural disorganization,” Finger said. “This suggests that both molecular and architectural changes may contribute to persistent taste dysfunction.”
Why does taste loss persist?
Taste bud cells are normally replaced every two to four weeks. But the researchers found evidence that cellular signaling disruptions may persist far longer in certain individuals.
While most COVID-19 patients recover their sense of taste within weeks or months, this study provides quantitative biological evidence explaining why recovery may be prolonged in a small group.
“Our findings offer measurable evidence of long-term taste disruption in some post-COVID patients long after the virus has been cleared,” the authors write.
Further research is needed to determine whether the molecular dysfunction can fully reverse and whether targeted therapies might restore normal taste signaling.
Key Questions Answered:
A: Taste isn’t a “one-size-fits-all” system. Salty and sour flavors enter your taste cells through simple ion channels. But sweet, bitter, and umami require a complex “G-protein” relay system. This study found that COVID-19 specifically breaks the “amplifier” (PLCβ2) for that relay, leaving the simple salt/sour channels untouched.
A: This is the big mystery the study highlights. Even though the cells are new, the “progenitor” cells (the ones making the new taste cells) seem to be producing “faulty” versions that lack the necessary signaling machinery. It’s like a factory that keeps putting out cars without engines.
A: Currently, no. But by identifying the specific protein (PLCβ2) that is missing, researchers can now look for targeted therapies—perhaps topical treatments or medications—to jumpstart the production of that specific protein and restore the signal.
Editorial Notes:
- This article was edited by a Neuroscience News editor.
- Journal paper reviewed in full.
- Additional context added by our staff.
About this Long-COVID and taste perception research news
Author: Laura Kelley
Source: University of Colorado
Contact: Laura Kelley – University of Colorado
Image: The image is credited to Neuroscience News
Original Research: Open access.
“Taste dysfunction in long COVID” by Hanna Morad , Tytti Vanhala , Marta A Kisiel , Agnes Andreason , Mei Li , Göran Andersson , Göran Laurell , Thomas E Finger , Göran Hellekant. Chemical Senses
DOI:10.1093/chemse/bjaf068
Abstract
Taste dysfunction in long COVID
Persistent taste dysfunction is frequently reported in individuals with post-acute sequelae of infection by SARS-CoV-2 (long COVID). The mechanisms and pathological correlates underlying this taste dysfunction are unknown.
This study investigates the underlying pathology in 28 non-hospitalized subjects diagnosed with COVID-19 who experienced taste disturbances more than 12 mo after testing positive for SARS-CoV-2.
To objectively establish the nature of the taste deficit, we used the WETT taste test, which quantifies the subject’s ability to taste each of the 5 taste qualities: sweet, umami, bitter, sour, and salty. We then biopsied 5 to 8 fungiform taste papillae (FP) in 20 of the 28 subjects.
The FPs were analyzed histologically for overall taste bud (TB) structure and innervation and by quantitative PCR (qPCR) for mRNA expression of markers for different taste receptor cells.
Although all subjects had reported taste dysfunction, only 3 showed overall taste scores below the 10th percentile for a normal population adjusted for age and sex. However, 11 of the 28 subjects exhibited total loss of one or more taste qualities.
Loss of PLCβ2-dependent taste qualities (sweet, umami, and bitter) was significantly more common and was correlated with reduced expression of PLCβ2 and Tas1R3 mRNAs. Histological analysis revealed generally preserved TB structure and innervation but with occasional disorganized TBs and abnormal, isolated PLCβ2-positive cells in the epithelium.
Our findings suggest long-term taste dysfunction after COVID-19 occurs rarely—more frequently involving PLCβ2-dependent taste qualities—but is not due to wholesale disruption of the taste periphery.
