COVID-19 Immunopathology

 SARS-CoV-2 has a tropism for ACE2-expressing epithelial cells of the respiratory tract, patients with severe COVID‑19 have symptoms of systemic hyperinflammation.

Pathogenesis of COVID-19

The ACE2 enzyme plays a vital role in the conversion of angiotensin Ang I to Ang-(1-9) and Ang II to Ang-(1-7) which have vasodilatory, antithrombotic and anti-inflammatory effects. The interaction of SARS-CoV-2 with ACE2 downregulates the anti-inflammatory function and increases angiotensin II effects in individuals who are predisposed. An initial immune response to the SARS-CoV-2 infection is triggered off by macrophages and dendritic cells with lymphocytosis and release of cytokine. The inflammatory response causes a destruction of the lymphocytes that are trying to defend against the virus, which results in lymphopenia. The production of cytokine rapidly becomes dysregulated and healthy cells are damaged, primarily the cells in the lungs but can involve other organs. The cytokine storm is presumed to be responsible for some of the severe manifestations of COVID-19. The cascade of damage associated with the cytokine storm disrupts the epithelial barrier, predisposing the lungs and other affected tissues to bacterial infection. Coagulation abnormalities ensues from the systemic inflammation and microcirculatory dysfunction caused by endotheliitis.

Tissue injury from COVID-19 can also occur via a direct cytotoxic effect. SARS-CoV-2 causes hypoxaemia which results in accumulation of oxygen free radicals, alteration in intracellular pH, accumulation of lactic acid, electrolyte imbalance and cellular damage.

. Clinical laboratory findings of elevated CRP ,LDH ,IL-2, IL-7, IL-6, granulocyte-macrophage colony-stimulating factor (GM-CSF), interferon-γ inducible protein 10 (IP-10), monocyte chemoattractant protein 1 (MCP-1), macrophage inflammatory protein 1-α (MIP-1α), and tumour necrosis factor-α (TNF-α) indicative of cytokine release syndrome (CRS) suggest an underlying immunopathology.

Additionally, people with COVID‑19 and acute respiratory distress syndrome (ARDS) have classical serum biomarkers of CRS, including elevated C-reactive protein (CRP), lactate dehydrogenase (LDH), D-dimer, and ferritin.

Systemic inflammation results in vasodilation, allowing inflammatory lymphocytic and monocytic infiltration of the lung and the heart. In particular, pathogenic GM-CSF-secreting T-cells were shown to correlate with the recruitment of inflammatory IL-6-secreting monocytes and severe lung pathology in COVID‑19 patients.

CRP means C Reactive Protein which is helpful marker in this inflammatory disease which increases in various inflammatory conditions but in relates to covid disease its very important. 

This Protein synthesized by liver.

CRP Increases in response to inflammation.It helps in their removal of dead or dying cells by binding.

CRP Value Increases in the TB,PNEUMONIA, autoimmune disease etc.

And in Normal conditions like pregnancy or oc pills,C REACTIVE PROTEIN values going to become high.

CRP test determine risk of heart disease 

C Reactive Protein Less than 1 is a low risk for heart disease. 

CRP 1 to 3 Which is a moderate or intermediate risk of developing heart disease 

More than 10....high risk for developing heart disease. But if patient having Cough,fever,loss of smell or taste sensations and increased CRP more than 10 is point towards COVID-19 infection more likely .

IL6 increases CRP. Inflammation subsiding then value of CRP going to  becomes normal.

IL6 is  estrogen hormone dependent.

Estrogen increases then IL6 Will decrease.