COVID-19 has quickly reached pandemic levels since it was first reported in December 2019. The virus responsible for the disease, named SARS-CoV-2, is enveloped positive-stranded RNA viruses. During its replication in the cytoplasm of host cells, the viral genome is transcribed into proteins, such as the structural protein spike domain S1, which is responsible for binding to the cell receptor of the host cells. Infected patients have initially flu-like symptoms, rapidly evolving to severe acute lung injury, known as acute respiratory distress syndrome (ARDS). ARDS is characterized by an acute and diffuse inflammatory damage into the alveolar-capillary barrier associated with a vascular permeability increase and reduced compliance, compromising gas exchange and causing hypoxemia. Histopathologically, this condition is known as diffuse alveolar damage which consists of permanent damage to the alveoli epithelial cells and capillary endothelial cells, with consequent hyaline membrane formation and eventually intracapillary thrombosis. All of these mechanisms associated with COVID-19 involve the phenotypic expression from different proteins transcription modulated by viral infection in specific pulmonary microenvironments. Therefore, this knowledge is fundamentally important for a better pathophysiological understanding and identification of the main molecular pathways associated with the disease evolution. Evidently, clinical findings, signs and symptoms of a patient are the phenotypic expression of these pathophysiological and molecular mechanisms of SARS-CoV-2 infection. Therefore, no findings alone, whether molecular, clinical, radiological or pathological axis are sufficient for an accurate diagnosis. However, their intersection and/or correlation are extremely critical for clinicians establish the diagnosis and new treatment perspectives.

自 2019 年 12 月首次报道以来，COVID-19 已迅速达到大流行水平。导致该疾病的病毒名为 SARS-CoV-2，是一种包膜正链 RNA 病毒。在宿主细胞的细胞质中复制期间，病毒基因组被转录成蛋白质，例如结构蛋白刺突结构域 S1，它负责与宿主细胞的细胞受体结合。受感染的患者最初有流感样症状，迅速发展为严重的急性肺损伤，称为急性呼吸窘迫综合征 (ARDS)。ARDS 的特征是肺泡-毛细血管屏障发生急性和弥漫性炎症损伤，伴有血管通透性增加和顺应性降低，影响气体交换并导致低氧血症。组织病理学上，这种情况被称为弥漫性肺泡损伤，包括对肺泡上皮细胞和毛细血管内皮细胞的永久性损伤，随后形成透明膜并最终形成毛细血管内血栓。所有这些与 COVID-19 相关的机制都涉及特定肺微环境中病毒感染调节的不同蛋白质转录的表型表达。因此，这些知识对于更好地理解和识别与疾病演变相关的主要分子途径具有根本性的重要意义。显然，患者的临床表现、体征和症状是SARS-CoV-2感染的这些病理生理和分子机制的表型表达。因此，无论是分子、临床、放射学或病理学轴足以进行准确诊断。然而，它们的交集和/或相关性对于临床医生建立诊断和新治疗观点极为关键。