It has become clear since the pandemic broke out that SARS-CoV-2 virus causes reduction of smell and taste in a significant fraction of COVID-19 patients. The olfactory dysfunction often occurs early in the course of the disease, and sometimes it is the only symptom in otherwise asymptomatic carriers. The cellular mechanisms for these specific olfactory disturbances in COVID-19 are now beginning to be elucidated. Several very recent papers contributed to explaining the key cellular steps occurring in the olfactory epithelium leading to anosmia/hyposmia (collectively known as dysosmia) initiated by SARS-CoV-2 infection. In this Viewpoint, we discuss current progress in research on olfactory dysfunction in COVID-19 and we also propose an updated model of the SARS-CoV-2-induced dysosmia. The emerging central role of sustentacular cells and inflammatory processes in the olfactory epithelium are particularly considered. The proposed model of anosmia in COVID-19 does not answer unequivocally whether the new coronavirus exploits the olfactory route to rapidly or slowly reach the brain in COVID-19 patients. To answer this question, new systematic studies using an infectious virus and appropriate animal models are needed.

中文翻译：

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COVID-19 中的嗅觉丧失：建立细胞机制的坎坷之路。

自大流行爆发以来，人们已经清楚地认识到，SARS-CoV-2 病毒会导致相当一部分 COVID-19 患者的嗅觉和味觉减弱。嗅觉功能障碍通常发生在病程早期，有时这是无症状携带者的唯一症状。COVID-19 中这些特定嗅觉障碍的细胞机制现在开始被阐明。最近的几篇论文有助于解释嗅觉上皮中发生的关键细胞步骤，导致 SARS-CoV-2 感染引发的嗅觉丧失/嗅觉减退（统称为嗅觉障碍）。在本观点中，我们讨论了 COVID-19 嗅觉功能障碍的研究进展，并提出了 SARS-CoV-2 引起的嗅觉障碍的更新模型。特别考虑了嗅觉上皮细胞中支持细胞和炎症过程的新兴核心作用。所提出的 COVID-19 嗅觉丧失模型并没有明确回答新型冠状病毒是否利用嗅觉途径快速或缓慢到达 COVID-19 患者的大脑。为了回答这个问题，需要使用传染性病毒和适当的动物模型进行新的系统研究。