Özet:

Coronoviruses (CoV) are zoonotic viruses that can infect many animal species in nature, including mammals and birds as well as human beings. The novel coronavirus, giving rise to COVID-19 pandemic since the beginning of 2020, has affected daily life shaking sociocultural and economic structure worldwide. CoV is an enveloped, single stranded RNA virus with positive polarity. Lung is the most affected organ in COVID-19. Spreading through respiratory droplets and direct contact, SARS-CoV-2 replicates first in the nasal cavity and pharenx, then proceed to lower respiratory tract. It has four major structural proteins: nucleocapsid protein (N), transmembrane protein (M), envelope protein (E) and spike protein (S). In order to enter a mammalian's cell, SARS-CoV-2 attaches to angiotensin converting enzyme2 (ACE2) receptor through S protein. The activity of cellular serine protease (TMMPRSS2) is also very important for this viral entry. The main target in the lungs are the type II pneumocytes. Present data shows that capillary endothelial cells in the lungs, highly expressing ACE-2 activity and sharing the same basal membrane with type II pneumocytes, are the other target cells. After the attachment of SARS-CoV-2 S protein, ACE-2 activity and surface expression diminishes. Loss of ACE-2 expression in the cell surface may lead to an instability in the renin-angiotensin system, causing a decrease in angiotensin II metabolism and increase in angiotensin II type 1a (ATIR) receptor stimulation. This may result in leakage from pulmonary blood vessels and severe acute lung damage. Covid-19 pneumonia is an atypical viral pneumonia. In level COVID-19 infection, viral immunosuppression may be due to lymphopenia, depletion of NK and CD8+ T cells and interferon suppression. After the delay of primary immune response, pro-inflammatory secondary immune response arises with excessive secretion of cytokines IL-6, IL-1, IP-10, IL-18, GM-CSF and IFNy, but no secretion of type I IFN. Continuous dissemination of viruses stimulates cytokine secretion and T cell response which induces lung injury and acute respiratory distress syndrome (ARDS).

Anahtar Kelimeler:

Özet:

Coronoviruses (CoV) are zoonotic viruses that can infect many animal species in nature, including mammals and birds as well as human beings. Novel coronavirus, giving rise to COVID-19 pandemic since the beginning of 2020, has affected daily life shaking sociocultural and economic structure worldwide. CoV is an enveloped, single stranded RNA virus with positive polarity. Lung is the most effected organ in COVID-19. Spreading through respiratory droplets and direct contact, SARS-CoV-2 replicates first in the nasal cavity and pharenx, then proceed to lower respiratory tract. It has four major structural proteins: nucleocapsid protein (N), transmembrane protein (M), envelope protein (E) and spike protein (S). In order to enter a mammalian’s cell, SARS-CoV-2 attaches to angiotensin converting enzyme2 (ACE2) receptor through S protein. The activity of cellular serine protease (TMMPRSS2) is also very important for this viral entry. Major target in the lungs are the type II pneumocytes. Present data shows that capillary endothelial cells in the lungs, highly expressing ACE-2 activity and sharing the same basal membrane with type II pneumocytes, are the other target cells. After the attachment of SARS-CoV-2 S protein, ACE-2 activity and surface expression diminishes. Loss of ACE-2 expression in the cellular surface may lead to an instability in the renin-angiotensin system, causing a decrease in angiotensin II metabolism and increase in angiotensin II type 1a (ATIR) receptor stimulation. This may result in leakage from pulmonary blood vessels and severe acute lung damage. Covid-19 pneumonia is an atypical viral pneumonia. In severe COVID-19 infection, viral immunosuppression may be due to lymphopenia, depletion of NK and CD8+ T cells and interferon suppression. After the delay of primary immune response, pro-inflammatory secondary immune response emerges with excessive secretion of cytokines IL-6, IL-1, IP-10, IL-18, GM-CSF and IFNy, but no secretion of type I IFN. Continuous dissemination of virus stimulates cytokine secretion and T cell response which induces lung injury and acute respiratory distress syndrome (ARDS).