ABSTRACT
Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is responsible for the coronavirus disease 2019 (COVID-19) pandemic that has become a significant global public health concern. The virus gains entry to cells via angiotensin-converting enzyme-2 (ACE2) receptors, which have been found to be the functional receptor for SARS-CoV-2 infection. High expression of ACE2 is found in type II alveolar cells, macrophages, bronchial and tracheal epithelial cells and in the oral cavity, particularly on the tongue. Taste disturbance is one of the early symptoms of COVID-19, suggesting that taste cells in taste buds are vulnerable to SARS-CoV-2 infection. Taste is modulated by hormones that are regulated in the renin-angiotensin-aldosterone system. Hypothetical causes of taste disturbance by SARS-CoV-2 may be due to direct cell and/or neuronal injuries, inflammatory responses and dysregulation of ACE2. © NZMA.
ABSTRACT
COVID-19 currently is a major pandemic disease in the world. It is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a member of the β-coronavirus genus that has 79% homology with severe acute respiratory syndrome (SARS) virus and can lead to acute respiratory infection. While COVID-19 patients typically present with respiratory symptoms such as fever, cough, some patients also report symptoms of digestive system. Studies have identified the SARS-CoV-2 RNA in stool specimens of infected patients, and the viral receptor angiotensin converting enzyme 2 (ACE2) is found to be expressed in gastrointestinal epithelial cells, hepatic cells and pancreatic cells, suggesting that fecal-mouth route is a potential route for transmission of SARS-CoV-2. This article reviewed the digestive manifestations and pathogenesis of patients with COVID-19.
ABSTRACT
Objective: To explore and analyze the possible mechanism of liver injury in patients with coronavirus disease 2019 (novel coronavirus pneumonia, NCP). Methods: The correlation between ALT, AST and other liver enzyme changes condition and NCP patients' disease status reported in the literature was comprehensively analyzed. ACE2 expression in liver tissue for novel coronavirus was analyzed based on single cell sequencing (GSE115469) data. RNA-Seq method was used to analyze Ace2 expression and transcription factors related to its expression in liver tissues at various time-points after hepatectomy in mouse model of acute liver injury with partial hepatectomy. t-test or Spearman rank correlation analysis was used for statistical analysis. Results: ALT and AST were abnormally elevated in some patients with novel coronavirus infection, and the rate and extent of ALT and AST elevation in severe NCP patients were higher than those in non-severe patients. Liver tissue results of single cell sequencing and immunohistochemistry showed that ACE2 was only expressed in bile duct epithelial cells of normal liver tissues, and very low in hepatocytes. In a mouse model of acute liver injury with partial hepatectomy, Ace2 expression was down-regulated on the first day, but it was elevated up to twice of the normal level on the third day, and returned to normal level on seventh day when the liver recovered and hepatocyte proliferation stopped. Whether this phenomenon suggests that the bile duct epithelial cells with positive expression of Ace2 participate in the process of liver regeneration after partial hepatectomy deserves further study. In RNA-Seq data, 77 transcription factors were positively correlated with the expression of Ace2 (r > 0.2, FDR < 0.05), which were mainly enriched in the development, differentiation, morphogenesis and cell proliferation of glandular epithelial cells. Conclusion: We assumed that in addition to the over activated inflammatory response in patients with NCP, the up-regulation of ACE2 expression in liver tissue caused by compensatory proliferation of hepatocytes derived from bile duct epithelial cells may also be the possible mechanism of liver tissue injury caused by 2019 novel coronavirus infection.