Summary: For a small subset of people with long COVID, flavors such as chocolate and coffee have been missing for more than a year. A new study now supplies direct biological evidence linking persistent taste loss to a specific molecular defect in human taste buds.
Researchers performing biopsies on human fungiform taste papillae found a pronounced drop in the messenger RNA (mRNA) that encodes the protein PLCβ2. PLCβ2 serves as an intracellular signal amplifier in taste receptor cells that detect sweet, bitter and umami tastes. When PLCβ2 is reduced, those taste signals are weakened to the point where the brain no longer registers them—even though the acute infection has resolved.
Key findings
- Amplifier defect: Quantitative PCR showed markedly reduced PLCβ2 mRNA in affected taste receptor cells, indicating loss of the protein that amplifies sweet, bitter and umami signals.
- Selective taste loss: The deficit primarily disrupted sweet, bitter and umami perception; salty and sour taste were largely preserved because they rely on different ion-channel pathways that do not depend on PLCβ2.
- Structural disorganization: Histological analysis revealed that some patients’ taste buds appeared physically disorganized, with occasional isolated PLCβ2-positive cells in the epithelium.
- Persistent signaling failure: Although taste receptor cells normally renew every two to four weeks, the molecular program that makes functional cells appears corrupted in some people for more than a year after infection.
- Direct biological link: This is the first study to tie long-term patient reports of taste loss to measurable molecular and structural abnormalities in human taste tissue.
Source: University of Colorado
Study overview
The study, published in Chemical Senses, examined 28 non-hospitalized individuals who reported persistent taste disturbances more than 12 months after a positive SARS-CoV-2 test. To quantify taste deficits, researchers used the WETT taste test, which measures sensitivity to the five basic taste qualities: sweet, umami, bitter, sour and salty. Biopsies of 5–8 fungiform papillae were taken from 20 of those participants for histological examination and quantitative PCR analysis of marker mRNAs for different taste receptor cell types.
Although self-reported taste dysfunction was common among the group, only a minority scored below the 10th percentile for global taste function after adjusting for age and sex. However, 11 of 28 subjects reported complete loss of one or more specific taste qualities. Losses affecting PLCβ2-dependent tastes (sweet, umami and bitter) were significantly more common and correlated with reduced expression of PLCβ2 and Tas1R3 mRNAs.
Molecular and structural details
The research team, including investigators from the University of Colorado Anschutz and Swedish universities, found that reduced PLCβ2 mRNA is a plausible molecular mechanism for selective taste loss. PLCβ2 functions within G-protein–coupled receptor signaling cascades that are essential for detecting sweet, bitter and umami compounds. Salty and sour taste transduction uses ion channels and therefore remains relatively unaffected when PLCβ2 levels fall.
Microscopic analysis showed that overall taste bud structure and innervation were generally preserved across subjects, but some biopsies displayed disorganized taste buds and abnormal distributions of PLCβ2-expressing cells. Those architectural changes could compound the functional impairment caused by the molecular defect.
Why the dysfunction can persist
One surprising observation is persistence of the defect despite rapid turnover of taste receptor cells. The study authors propose that progenitor cells responsible for generating new taste receptor cells may themselves carry altered gene expression programs after infection, repeatedly producing cells that lack the necessary signaling apparatus. In other words, the “factory” that builds taste cells appears to be producing defective units for an extended period.
The corresponding author, Thomas Finger, PhD, describes PLCβ2 as a molecular amplifier inside taste cells: when its levels are reduced, the taste signal sent to the brain is weakened. The findings therefore offer measurable evidence that long-term taste disruption can persist in some post-COVID patients long after the virus is cleared.
Clinical implications and next steps
There is currently no established cure for persistent post-COVID taste loss. By identifying a specific molecular target—PLCβ2—this study points toward possible future interventions that could aim to restore expression of the missing protein or otherwise boost the affected signaling pathway. Potential approaches might include targeted pharmacologic agents or topical treatments to stimulate the relevant gene programs, but clinical trials will be needed to assess safety and efficacy.
Further research should clarify how often this mechanism occurs among all people with long COVID, whether it fully reverses over time, and which therapeutic strategies can restore normal taste signaling.
Key questions answered
A: Salty and sour tastes use simple ion channels that do not depend on PLCβ2. Sweet, bitter and umami rely on a G-protein relay that requires PLCβ2 as an amplifier; when PLCβ2 expression is reduced, those tastes become weak or undetectable.
Q: If taste cells regenerate monthly, why hasn’t taste returned?
A: The study suggests progenitor cells that make new taste receptor cells may remain altered after infection, repeatedly producing cells that lack the necessary signaling machinery—like a factory repeatedly assembling a product missing a key component.
Q: Is there a cure for long COVID taste loss?
A: Not yet. Identifying PLCβ2 as a specific missing component provides a clear target for future research into therapies designed to restore the molecular machinery of taste receptor cells.
Editorial notes
- This article was edited by an editor at Neuroscience News.
- The original journal paper was reviewed in full by the reporting team.
- Additional context was added by staff based on the published findings.
About this research
Author: Laura Kelley (University of Colorado)
Source: University of Colorado
Contact: Laura Kelley – University of Colorado
Image: Image 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 (summary)
Persistent taste dysfunction is frequently reported among individuals with post-acute sequelae of SARS-CoV-2 infection (long COVID), but the underlying mechanisms were unclear. This study assessed 28 non-hospitalized people with taste disturbances more than 12 months after COVID-19 and performed biopsies on 20 participants. Objective taste testing showed that specific loss of PLCβ2-dependent tastes (sweet, umami and bitter) was common and correlated with reduced PLCβ2 and Tas1R3 mRNA expression. Histology showed generally preserved taste bud structure and innervation, with occasional disorganized taste buds and abnormal PLCβ2-positive cells in the epithelium. The findings indicate that long-term taste dysfunction after COVID-19 is uncommon but, when it occurs, often involves PLCβ2-dependent taste qualities without wholesale destruction of the taste periphery.