Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has a marked tropism for the biliary tract; it damages the bile ducts and hepatocytes and can lead to liver decompensation, cirrhosis, and sepsis. The pathogenesis of liver damage and its association with damage to the lung, heart, and brain and to the other protean manifestations of COVID-19 disease are not fully understood. In particular, tissue damage from thinning and leaky blood vessels appears to result from an inflammatory response to the virus rather than the virus itself. This article outlines a new hypothesis of the nature of the inflammatory factor responsible for tissue damage in COVID-19. Review of the literature reveals that COVID-19 disease closely resembles an endogenous form of hypervitaminosis A. We propose that SARS-CoV-2 virus-induced liver damage causes retinoic acid and stored retinyl esters to be released into the circulation in toxic concentrations, unbound to protein, with resulting damage to organs including the lungs, heart, blood vessels, and skin. Several lines of evidence support this model of disease causation. Subject to testing, strategies for the effective treatment and prevention of COVID-19 could include targeting the action and accumulation of retinoids.

中文翻译：

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COVID-19 疾病发病机制中的肝损伤和暴露于有毒浓度的内源性维甲酸：假设

严重急性呼吸系统综合症冠状病毒 2 (SARS-CoV-2) 对胆道有明显的趋向性；它会损害胆管和肝细胞，并可能导致肝功能失代偿、肝硬化和败血症。肝损伤的发病机制及其与肺、心脏和脑损伤以及 COVID-19 疾病的其他多变表现的关系尚不完全清楚。特别是，血管变薄和渗漏造成的组织损伤似乎是由对病毒而非病毒本身的炎症反应引起的。本文概述了导致 COVID-19 组织损伤的炎症因子的性质的新假设。文献回顾表明，COVID-19 疾病与维生素 A 过多症的内源性形式非常相似。我们提出，SARS-CoV-2 病毒引起的肝损伤会导致视黄酸和储存的视黄酯以有毒浓度释放到循环中，未与蛋白质结合，从而对肺、心脏、血管和皮肤等器官造成损害. 有几条证据支持这种疾病因果关系模型。根据测试，有效治疗和预防 COVID-19 的策略可能包括针对类视黄醇的作用和积累。