COVID-19, mainly manifested as acute respiratory distress syndrome, has afflicted millions of people worldwide since 2019. Taste dysfunction is a common early-stage symptom of COVID-19 infection that burdens patients for weeks or even permanently in some cases. Owing to its subjectivity and complexity, the mechanism of taste disorder is poorly studied. Previous studies have reported that the COVID-19 entry receptors are highly expressed in taste buds, thereby intensifying the cytocidal effect. Taste receptor cells are vulnerable to inflammation, and the COVID-19-induced cytokine storm causes secondary damage to taste function. Interferon and various proinflammatory cytokines can trigger cell apoptosis and disrupt the renewal of taste bud stem cells. This immune response can be further enhanced by the accumulation of Angiotensin II (Ang II) caused by an unbalanced local renin-angiotensin system (RAS) system. In addition, severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) is neurotropic and can invade the brain through the olfactory bulb, affecting the nervous system. Other factors, such as host zinc deficiency, genetic susceptibility, sialic acid, and some neurotransmitters, also contribute to the pathogenesis process. Although several medical interventions have displayed effectiveness, only a few strategies exist for the treatment of postinfectious dysgeusia. Stem cell-based taste regeneration offers promise for long-term taste disorders. Clinical studies have demonstrated that stem cells can treat long COVID-19 through immune regulation. In dysgeusia, the differentiation of taste bud stem cells can be stimulated through exogenous epithelial-derived and neural-derived factors to regenerate taste buds. Tongue organoids are also emerging as functional taste buds, offering new insights into the study of taste regeneration. This review presents the current evidence of the pathogenesis of COVID-19-related dysgeusia, summarizes currently available treatments, and suggests future directions of taste regeneration therapy.

中文翻译：

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COVID-19 相关味觉障碍的发病机制和治疗。

COVID-19 主要表现为急性呼吸窘迫综合征，自 2019 年以来已困扰着全球数百万人。味觉功能障碍是 COVID-19 感染的常见早期症状，在某些情况下会给患者带来数周甚至永久性的负担。由于其主观性和复杂性，味觉障碍的机制研究较少。此前的研究报告称，COVID-19进入受体在味蕾中高表达，从而增强了杀细胞作用。味觉感受器细胞容易受到炎症的影响，而COVID-19引发的细胞因子风暴会对味觉功能造成二次损害。干扰素和各种促炎细胞因子可以引发细胞凋亡并破坏味蕾干细胞的更新。这种免疫反应可以通过局部肾素-血管紧张素系统（RAS）系统不平衡引起的血管紧张素II（Ang II）的积累进一步增强。此外，严重急性呼吸综合征冠状病毒2型（SARS-CoV-2）具有嗜神经性，可通过嗅球侵入大脑，影响神经系统。其他因素，如宿主缺锌、遗传易感性、唾液酸和一些神经递质，也有助于发病过程。尽管一些医疗干预措施已显示出有效性，但治疗感染后味觉障碍的策略却很少。基于干细胞的味觉再生为长期味觉障碍提供了希望。临床研究表明，干细胞可以通过免疫调节来治疗长期的COVID-19。在味觉障碍中，可以通过外源性上皮源性和神经源性因子刺激味蕾干细胞的分化，从而再生味蕾。舌类器官也作为功能性味蕾出现，为味觉再生研究提供了新的见解。本综述介绍了与 COVID-19 相关的味觉障碍发病机制的当前证据，总结了当前可用的治疗方法，并提出了味觉再生治疗的未来方向。