• Cristina CIJEVSCHI PRELICEAN “Grigore T. Popa” University of Medicine and Pharmacy Iasi
  • Cătălina MIHAI “Grigore T. Popa” University of Medicine and Pharmacy Iasi


Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) belongs to the coronaviruses family, being the 7th virus of the family (1). The disease caused by SARS-CoV-2 is called “corona virus disease 2019 –COVID 19”. Coronaviruses are responsible for severe acute respiratory syndrome coronavirus (SARS), the Middle Eastern respiratory syndrome coronavirus (MERS). The new coronavirus, SARS-CoV-2, is responsible for the current pandemia. It is an ARN virus which, by frequent mutations, has the capacity to decrease or increase its transmissibility and pathogeny. It is transmitted mainly by the respiratory tract, by air and by secretions, but it was also demonstrated the possibility of fecal-oral transmission (2). The main symptoms are fever, cough, asthenia, dyspnea, anosmia, ageusia. In about 50% of cases can occur digestive manifestations (3). The majority of patients have mild or moderate forms of the disease, but in 5% of cases these can be severe, leading to the patient’s death, especially in elderly people with comorbidities (hypertension, diabetes, ischemic heart disease). The virus SARS-CoV-2 enters human cells by means of receptors: the angiotensin-converting enzyme 2 (ACE2), trans - membrane protease serine 2 (TMPRRS2) and, for certain strains, dipeptidyl peptidase-4 (DPP4) (4). ACE2 is considered to be the main receptor and it is to be found both in soluble form in serum and on the level of the epithelial cells from the respiratory, digestive, urinary tract. When the viral spike protein enters ACE2, together with ACE2 cleavage by TMPRSS2, it is facilitated the penetration of the virus into the cell, viral replication and intercellular transmission. ACE2 transforms angiotensin II into angiotensin 1-7. This acts upon Mas receptors inducing vasodilation, increases renal elimination of water and sodium and has an anti-inflammatory effect by means of the nitric oxide. Binding virus to ACE2 causes a decrease in angiotensin 1-7 with an increase in angiotensin II responsible for the occurrence of immune mediated inflammation and the injury of the parenchyma (5).

Author Biographies

Cristina CIJEVSCHI PRELICEAN, “Grigore T. Popa” University of Medicine and Pharmacy Iasi

Institute of Gastroenterology and Hepatology,
“Sf. Spiridon” County Clinical Emergency Hospital Iasi

Cătălina MIHAI, “Grigore T. Popa” University of Medicine and Pharmacy Iasi

Institute of Gastroenterology and Hepatology,
“Sf. Spiridon” County Clinical Emergency Hospital Iasi


1. Wu Di, Wu T, Liu Q, Yang Z. The SARS-CoV-2 outbreak: What we know. Intern J Inf Dis 2020; 94: 44-48.
2. Amirian ES. Potential fecal transmission of SARS-CoV-2: Current evidence and implications for public health. Intern J Inf Dis 2020; 95: 363-370.
3. Aguila EJT, Cua IHY, Dumagpi JEL, et al. COVID 19 and its effects on the digestive system and endoscopy practice. J Gastroenterol Hepatol 2020: 4: 324-331.
4. Hoffmann M, Kleine-Weber H, Schroeder S, et al. SARS-CoV-2 cell entry depends on ACE2 and TMPRSS2 and is blocked by clinically proven protease inhibitor. Cell 2020; 181(2): 271-280.e8.
5. Li LY, Wu W, Chen S, et al. Digestive system involvement of novel coronavirus infection: Prevention and control infection from a gastroenterology perspective. J Dig Dis 2020; 21: 199-204.
6. Huang C, Wang Y, Li X, et al. Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China. Lancet 2020; 395: 497-506.
7. Wong SH, Lui RN, Sung JJ. COVID-19 and the digestive system. J Gastroenterol Hepatol 2020; 35(5): 697-905.
8. Xu H, Zhong L, Deng J, et al. High expression of ACE2 receptor of 2019-n CoV on the epithelial cells of oral mucosa. Int J Oral Sci 2020; 12(1): 8-12.
9. Ma C, Cong Y, Zhang H. COVID-19 and the Digestive System. Am J Gastroenterol 2020;10.14309/ajg.0000000000000691.
10. Wu Y, Guo C. Tang L, et al. Prolonged presence of SARS-CoV-2 viral RNA in fecal samples. Lancet Gastroenterol Hepatol 2020; 5: 434-435.
11. Tian Y, Rong L, Nian W, He Y. Review article: gastrointestinal features in COVID-19 and the possi-bility of fecal transmission. Aliment Pharmacol Ther 2020; 51: 843-851.
12. Bahayana R, Som A, Li MD, et al. Abdominal Imaging Findings in COVID-19: Preliminary Observa-tions. Radiology 2020.
13. Xu L, Liu J, Yang D, Zheng X. Liver injury during highly pathogenic human coronavirus infections. Liver Int 2020; 40(5): 998-1004.
14. Guan WJ, Ni ZY, Hu Y, et al. Clinical characteristics of coronavirus disease 2019 in China. N Engl J Med 2020; 382: 1708-1720.
15. Xu Z, Shi L, Wang Y, et al. Pathological findings of COVID -19 associated with acute respiratory distress syndrome. Lancet Respir Med 2020; 8(4): 420-422.
16. Gralnek IM, Hassan C. Beilenhoff U, et al. ESGE and ESGENA position statement on gastrointestinal endoscopy and the COVID -19 pandemic. Endoscopy 2020; 52: 483-490.
17. Kennedy NA, Jones GR, Lamb CA, et al. British Society of Gastroenterology guidance for manage-ment inflammatory bowel disease during COVID-19 pandemic. Gut 2020; 69: 984-990.
18. Mao R, Liang J, Shen J, et al. Implications of COVID-19 for patients with pre-existing digestive diseases. Lancet Gastroenterol Hepatol 2020; 5(5): 425-427.
19. Boetler T, Newsome PN, Mondelli MU, et al. Care of patients with liver disease during COVID-19 pandemic: EASL-ESCMID position paper. JHEP Rep 2020; 2: 100113-100117.
20. Gheorghe C. Clinical Insights for gastroenterology and Hepatology Providers during COVID-19 Pandemic. J Gastrointest Liver Dis 2020; 29(2): 131-134.