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Introduction
• Coronavirus are large, enveloped, single stranded RNA
virus found in humans, dogs, cats, birds, bats.
• It ...
Target cells
• Nasal and bronchial epithelial cells
• Type I and type II pneumocytes
• Endothelial cells of pulmonary capi...
Pathophysiology
Pathophysiology
1. SARS-CoV-2 enters into the nasal cavity via aerosol transmission.
2. It will bind to ACE2 on the nasal ...
8. There is migration of the virus from the nasal epithelium to the upper
respiratory tract via the conducting airways.
9....
Inflammatory mechanisms, alveolar epithelial
and endothelial damage, and coagulopathy in
COVID-19
15. This cytokine storm will act as a chemoattractant for
neutrophils, CD4 helper T cells and CD8 cytotoxic T cells which
...
Subscribe to our channel- HM
Learnings
Pathophysiology of COVID-19 Part 1 (SARS CoV 2) I Target cells of COVID 19 I Coronavirus life cycle I
Pathophysiology of COVID-19 Part 1 (SARS CoV 2) I Target cells of COVID 19 I Coronavirus life cycle I
Pathophysiology of COVID-19 Part 1 (SARS CoV 2) I Target cells of COVID 19 I Coronavirus life cycle I
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Pathophysiology of COVID-19 Part 1 (SARS CoV 2) I Target cells of COVID 19 I Coronavirus life cycle I

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Pathophysiology of COVID-19 Part 1 (SARS CoV 2) I Target cells of COVID 19 I Coronavirus life cycle I
The slides will be about the following:
1. Introduction
2. Target cells of COVID
3. Pathophysiology of SARS-CoV - nasal cavity, upper respiratory tract, alveoli

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Pathophysiology of COVID-19 Part 1 (SARS CoV 2) I Target cells of COVID 19 I Coronavirus life cycle I

  1. 1. Introduction • Coronavirus are large, enveloped, single stranded RNA virus found in humans, dogs, cats, birds, bats. • It has a diameter of 90-140nm and a spike , ranging from 9nm to 12nm .
  2. 2. Target cells • Nasal and bronchial epithelial cells • Type I and type II pneumocytes • Endothelial cells of pulmonary capillaries.
  3. 3. Pathophysiology
  4. 4. Pathophysiology 1. SARS-CoV-2 enters into the nasal cavity via aerosol transmission. 2. It will bind to ACE2 on the nasal epithelial cells. ACE2 is the main host cell receptor for viral entry into the cells and have a high expression on the nasal epithelial cells. 3. The type 2 transmembrane serine protease (TMPRSS2)/ transmembrane protease serine 2 present on the host cell activate S (spike) protein on the coronavirus and it will bind to ACE2 receptor. 4. This will lead to cleavage of ACE2 and uptake of virus by the endocytosis inside the host cell. 5. Virus will release its RNA inside the cell and RNA will take over the cell machinery to replicate itself and assemble more viruses. 6. These replicated virions will be released and infect the adjacent cells. 7. Limited immune response when virus is in nasal cavity. (asymptomatic)
  5. 5. 8. There is migration of the virus from the nasal epithelium to the upper respiratory tract via the conducting airways. 9. Clinical features (fever, cough, malaise) manifest. Innate immune response occurs when virus is in upper respiratory tract- release of CXCL10 (chemokine ligand-10) and interferons (IFN-β and IFN-λ) from infected cells. 10. Virus disseminates into the lower respiratory tract by either (micro- )aspiration of SARS-CoV-2 particles causes spread from the oropharynx to the lungs (propagated by infecting the ciliated cells) or the airborne microparticles are transported directly into the lower respiratory tract by airflow, bypassing the upper airways. 11. Reaching the alveoli, it will target alveolar cells especially type II pneumocytes and also the lung endothelial cells. 12. Invade these cells by the same process via ACE2 receptor and replicate and progress the infection. 13. Inflammatory signaling molecules (cytokine storm) are released by infected cells and alveolar macrophages to recruited T lymphocytes, monocytes, and neutrophils at site of injury. 14. Cytokine storm consists of interleukins (IL-1, IL-6, IL-8, IL-120 and IL-12), tumour necrosis factor-α (TNF-α), IFN-λ and IFN-β, CXCL-10, monocyte chemoattractant protein-1 (MCP-1) and macrophage inflammatory protein-1α (MIP-1α).
  6. 6. Inflammatory mechanisms, alveolar epithelial and endothelial damage, and coagulopathy in COVID-19
  7. 7. 15. This cytokine storm will act as a chemoattractant for neutrophils, CD4 helper T cells and CD8 cytotoxic T cells which will reach the site of injury by diapedesis. 16. These immune cells will fight and try to kill the virus but in doing so it further increase the inflammation and lung injury. 17. As the disease progresses, tissue and plasma kallikreins break the kininogen into kinin which will bind to its receptor on lung endothelium, resulting in vascular smooth muscle relaxation and increase in capillary permeability leading to pulmonary edema. 18. Progression of viral injury along with the host inflammatory response leads to the damage of alveolar wall and epithelial endothelial barrier integrity. 19. This widespread acute inflammation, lung injury, alveolar edema and alveolar damage leads to acute respiratory distress syndrome. 20. ARDS is characterized by bilateral lung infiltrates and severe progressive hypoxemia.
  8. 8. Subscribe to our channel- HM Learnings
  • arpitaurukuzhil

    Jun. 24, 2021
  • SManasa2

    Jun. 21, 2021
  • AtulSangewar

    May. 23, 2021
  • HMLearnings

    May. 9, 2021

Pathophysiology of COVID-19 Part 1 (SARS CoV 2) I Target cells of COVID 19 I Coronavirus life cycle I The slides will be about the following: 1. Introduction 2. Target cells of COVID 3. Pathophysiology of SARS-CoV - nasal cavity, upper respiratory tract, alveoli

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