Chiba Cancer Center, 666-2 Nitonacho, Chuouku, Chiba City, Chiba 260-8717, Japan.
Med Hypotheses. 2020 Nov;144:110020. doi: 10.1016/j.mehy.2020.110020. Epub 2020 Jun 20.
Pulmonary surfactant is considered to be one of the soaps. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and the other enveloped viruses become very weak against surfactant. The SARS virus binds to angiotensin-converting enzyme (ACE2) receptor and causes pneumonia. In the lung, the ACE2 receptor sits on the top of lung cells known as alveolar epithelial type II (AE2) cells. These cells play an important role in producing surfactant. Pulmonary surfactant is believed to regulate the alveolar surface tension in mammalian lungs. To our knowledge, AE2 cells are believed to act as immunoregulatory cells; however, pulmonary surfactant itself has not been believed to act as a defender against the enveloped viruses. This study hypothesises that pulmonary surfactant may be a strong defender of enveloped viruses. Therefore, old coronaviruses merely cause pneumonia. On the contrary, new SARS-CoV-2 can suppress the production of surfactant that binds to the ACE2 of AE2 cells. The coronavirus can survive in the lung tissue because of the exhaustion of pulmonary surfactant.
肺表面活性剂被认为是肥皂的一种。严重急性呼吸综合征冠状病毒 2（SARS-CoV-2）和其他包膜病毒对肺表面活性剂变得非常脆弱。SARS 病毒与血管紧张素转换酶（ACE2）受体结合，导致肺炎。在肺部，ACE2 受体位于称为肺泡上皮 II 型（AE2）细胞的肺细胞顶部。这些细胞在产生肺表面活性剂方面发挥着重要作用。肺表面活性剂被认为可以调节哺乳动物肺部的肺泡表面张力。据我们所知，AE2 细胞被认为是免疫调节细胞；然而，肺表面活性剂本身并不被认为是针对包膜病毒的防御者。本研究假设肺表面活性剂可能是包膜病毒的强大防御者。因此，旧的冠状病毒仅引起肺炎。相反，新型 SARS-CoV-2 可以抑制与 AE2 细胞的 ACE2 结合的肺表面活性剂的产生。由于肺表面活性剂的耗尽，冠状病毒可以在肺组织中存活。
