Long COVID Taste Loss Linked to Reduced PLCβ2 and TAS1R3 Expression

Persistent taste alteration after SARS-CoV-2 infection is reported as a long-term symptom for some patients and, in a small proportion, can persist for months. A recent report described long-standing dysgeusia with modality-specific deficits on objective taste testing and reported lower expression of selected type II taste-cell markers in sampled tongue papillae; correlations with taste scores were limited (the combined sweet+umami average, but not sweet or umami alone, correlated with mRNA expression). In that account, psychophysical findings and tissue-based assays are presented side by side as correlates of ongoing gustatory complaints rather than as isolated observations. The emphasis is on describing psychophysical and tissue-level correlates that accompany persistent taste change after COVID-19.

Sampling focused on fungiform papillae (taste-bud–containing epithelium) obtained by biopsy in a subset of participants, with microscopic review and quantitative mRNA measurement used to characterize the peripheral taste apparatus. The authors reported lower mRNA expression of PLCβ2 and TAS1R3 in taste-bud samples from individuals with persistent post-COVID taste dysfunction, framing these as markers linked to type II taste receptor-cell signaling. In a separate description, most papillae appeared grossly normal on inspection, while a minority showed disorganized structure and isolated PLCβ2-positive cells within the epithelium on histologic assessment. The tissue workup is presented as a molecular and structural snapshot consistent with altered type II taste-cell marker expression in this cohort.

Objective psychophysical assessment was reported using WETT, which provides quantitative measures across the five basic tastes and allows inspection of modality-level patterns rather than relying only on symptom report. In the described cohort, many participants showed preferential impairment affecting sweet, umami, and bitter perception, while sour and salty were less emphasized in the overall pattern. The report highlighted a scoring nuance: an overall composite score can fall within an age- and sex-adjusted normative range even when one or more individual taste modalities are absent or markedly reduced, underscoring the difference between global and modality-specific readouts. This psychophysical profile is presented as aligning with the paper’s focus on PLCβ2-mediated taste modalities without requiring that all taste qualities be uniformly affected.

Virology testing of sampled papillae was described as negative for detectable viral RNA despite persistent dysfunction, a finding the authors discussed in the context of ongoing symptoms after presumed viral clearance. Proposed explanations were framed as hypotheses, including longer-lasting molecular changes (described with the term “inflammatory memory”) and the possibility of disrupted nerve–taste cell connectivity or nerve transmission affecting function even when gross anatomy appears largely preserved. Design caveats were also noted: the study was described as a single-timepoint retrospective cohort without pre-infection taste measurements for within-person comparison.

Key Takeaways:

• The authors reported lower PLCβ2 and TAS1R3 mRNA expression in taste-bud tissue from individuals with persistent post-COVID taste dysfunction.
• Psychophysical testing was described as showing selective losses (often sweet, umami, and bitter) and noted that composite scores can appear normal despite modality-specific deficits.
• Viral RNA was reported as not detected in sampled papillae, and the authors discussed hypotheses (including “inflammatory memory” and disrupted connectivity) alongside single-timepoint design limitations.