ISSN: 0976-3031
Research Article
PATHOGENESIS OF COVID-19 AND THE BODY'S RESPONSES
Giulio Tarro
President of the T&L de Beaumont Bonelli Foundation for Cancer Research, Italy
DOI: http://dx.doi.org/10.24327/ijrsr.2020.1103.5209 ARTICLE INFO ABSTRACT
Children are infected with the virus without suffering a serious disease and represent an important source of infection. It has been experimentally proven that young mice respond to lung tissue damage from viral infection through prostaglandins, while adult mice succumb. The angiotensinconverting enzyme (ACE) 2 receptor is particularly abundant on the cells of the lower lung pathways, whose situation explains the high incidence of bronchitis and pneumonia related to the severe infection of COVID-19. A fall in ACE2 activity in the elderly is partly responsible for the decreased ability to reduce the inflammatory response with old age. The reduction of ACE2 receptors in older adults puts them in a position where they are unable to cope with COVID-19. In Italy from the details of the medical records of the current hospitalized as well as those discharged healed and unfortunately the victims do not seem to have any foreigner in the sense of a non-EU citizen.Non-EU citizens are all covered by a tuberculosis vaccine which is part of a coverage protocol provided by the Local Health Unit.It seems that flu vaccination favors coronavirus infection, even greater than 36% as reported by an American military study. Both meningococcal and pneumociccic disease have been associated with the activity of influenza and respiratory syncytial viruses.The Istituto Superiore della Sanità recently stated that few deaths are from coronavirus and instead most put of them from other pathologies (cardiovascular, cancer, diabetes, etc.). This suggests that the overall clinical consequences of COVID-19 could ultimately be similar to that of severe seasonal flu, which has a fatality rate of approximately 0.1%, or pandemic influenza such as that of 1957 or 1968. , rather than those of SARS or MERS, characterized respectively by a fatality of 10% and 36%.
INTRODUCTION
According to the experience of the first SARS and of the MERS, the children were not exposed to the civet cat and camels in a similar way (1).It was thought that the same fact could take place with the SARS from COVID-19 (2). Indeed children are infected with the virus without suffering a serious disease and represent an important source of infection. The virus is found in their rectal swabs.
Growing with age many specific cells of the immune system are no longer active and therefore the body loses its ability to respond effectively. In fact, it has been experimentally proven that young mice respond to lung tissue damage from viral infection through prostaglandins, while adult mice succumb. The juvenile immune system and its efficient T Helper cells respond to SARS COVID 2. The Helper cell's CD4 lymphocytes stimulate B cells to produce antibodies against the virus and control infection. In this case Th2 lymphocytes are able to control the inflammatory response caused by the viral infection, preventing an exuberant and delayed reaction as occurs in adults. The different hormonal structure and the same proglandins favor the female subject against the coronavirus responsible for the current pandemic.
Another important discussion concerns the ACE2 receptor, that is, the angiotensin-converting enzyme 2. Both the first SARS and the current SARS have the same cellular entry route through this receptor for coronaviruses (3). The receptor is particularly abundant on the cells of the lower lung pathways, whose situation explains the high incidence of bronchitis and pneumonia related to the severe infection of COVID-19(4). The same receptor is abundantly represented on the mouth and tongue facilitating the viral entry of the host organism. Despite its reduction with adulthood, the ACE2 enzyme is an important regulator of the immune response, in particular inflammation protects mice against acute lung damage triggered by sepsis. In 2014 it was shown that the ACE2 enzyme protects against lethal avian influenza. Some of the best-performing patients had high levels of the protein in their serum. By blocking the gene for ACE2, severe lung
Available Online at http://www.recentscientific.com International Journal of Recent Scientific Research International Journal of Recent Scientific Research Vol. 11, Issue, 03 (D), pp. 37940-37942, March, 2020
Copyright © Giulio Tarro, 2020, this is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution and reproduction in any medium, provided the original