SARS-CoV-2 INFECTION: GASTROENTEROLOGIST POINT OF VIEW
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).
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