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Severe Acute Respiratory Syndrome Coronary Virus-2 (SARS-CoV-2) is a highly contagious respiratory virus that can cause venous/arterial thromboembolism, stroke, kidney failure, myocardial infarction, platelet reduction, and other terminal organ damage.
Based on end-organ protection in the C3 defective mouse model, coupled with evidence of complement activation in the human body, the researchers were given the guess that SARS-CoV-2 could trigger endostro cord damage mediated by complements, but the mechanism was unclear.
study, the researchers confirmed that SARS-CoV-2's echizor protein (1 and 2 sub-units), rather than N protein, directly activates the complement's alternative pathway (APC).
improved Ham test, complement-dependent lethality can be blocked by C5 or D factor suppression.
S proteins of SARS-CoV-2 1 sub-unit (S1), echithoprotein 2 sub-units (S2) and HCoV-OC43 can increase the deposition of C5-9b. However, the nuclear shell (N) protein of SARS-CoV-2 could not be deposited in C3 fragments and C5b-9 on TF1PIGAnull target cells, and the amount of complement factor Bb in the upper fluid of the echithoprotein-treated cells increased.
C5 inhibition can block the accumulation of C5b-9 on cells, but it can not block the accumulation of C3c, but D-factor inhibition can block the accumulation of C3c and C5b-9 at the same time.
add an H factor to reduce complement attacks.
simulation of COVID-19, SARS-CoV-2's echithrin converts an inactive surface into an active surface by inhibiting APC conversion enzyme inactivation on the cell surface.
APC activates or explains many clinical manifestations in patients with COVID-19 (microvascular lesions, plate plate plate reduction, kidney damage, and thrombosis tendencies), these symptoms are also found in other supplement-driven diseases, such as atypical hemolytic uremia syndrome and catastrophic antiphospholipid antibody syndrome.
C5 inhibition prevents the accumulation of C5b-9, but does not block upstream complement activation caused by SARS-CoV-2 echithrin.
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