Production: Pablo Cantudo
The SARS-CoV-2 or new coronavirus was detected three months ago in humans, and today it affects about 250,000 people worldwide. Almost 200 scientific publications issued since its discovery attempt to describe its epidemiology in detail, in order to develop safe and effective drugs and vaccines.
For now, we know that the virus that causes COVID-19 is covered with spikes and has an oily lipid that dissolves in contact with soap. SARS-CoV-2 enters the body through the mouth, nose or eyes, through the tiny droplets that humans expel when we speak, laugh, cough or sneeze.
For now, we know that the virus that causes the COVID-19 disease, SARS-CoV-2, has on its surface proteins, called ACE2, that have a specific affinity with receptors on the cells of the pulmonary alveoli. The alveoli are like small bags that fill with air located at the end of the bronchi; Well, the cells of the alveoli have ACEII receptors, which would facilitate the entry of the virus into the cells. That is why we know why the lung is the organ most affected by infection; but these receptors would also be present in other tissues of the body, such as the intestine.
Upon entering the body through the respiratory tract, the virus fuses with lung cells, releasing the genetic material RNA. Through proteins, SARS-CoV-2 ‘convinces’ the immune system that everything is fine. while new copies of the virus are created inside the cell. By the time the new strains of SARS-CoV-2 are ready to leave the cell, millions of copies have been made. Then the infected host cell dies.
People with COVID-19 develop symptoms such as a cough, fever, and shortness of breath as the immune system recovers, trying to fight the virus. In some cases, the immune system can attack healthy cells in the lung. A small percentage of infections can lead to serious complications or even death.
When studying similar coronaviruses such as SARS-CoV, which causes Severe Acute Respiratory Syndrome (or simply SARS), it was found that the pointed proteins of SARS-CoV-2 and the coronavirus that causes severe acute respiratory syndrome (SARS) have structures nearly identical three-dimensional. That is, both viruses would use the same strategy to enter lung cells. Of course, scientists believe that SARS-CoV-2 recognizes human ACE2 more efficiently than SARS-CoV; that would explain its rapid and powerful spread.
