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COVID-19: A collision of complement, coagulation and inflammatory pathways

wastwater

Senior Member
Messages
1,271
Location
uk
https://onlinelibrary.wiley.com/doi/10.1111/jth.14981

Abstract

COVID-19 is frequently accompanied by a hypercoagulable inflammatory state with microangiopathic pulmonary changes that can precede the diffuse alveolar damage characteristic of typical acute respiratory distress syndrome (ARDS) seen in other severe pathogenic infections. Parallels with systemic inflammatory disorders such as atypical hemolytic uremic syndrome (aHUS) have implicated the complement pathway in the pathogenesis of COVID-19, and particularly the anaphylatoxins C3a and C5a released from cleavage of C3 and C5, respectively. C5a is a potent cell signalling protein that activates a cytokine storm—a hyper-inflammatory phenomenon—within hours of infection and the innate immune response. However, excess C5a can result in a pro-inflammatory environment orchestrated through a plethora of mechanisms that propagate lung injury, lymphocyte exhaustion, and an immune paresis. Furthermore, disruption of the homeostatic interactions between complement and extrinsic and intrinsic coagulation pathways contributes to a net pro-coagulant state in the microvasculature of critical organs. Fatal COVID-19 has been associated with a systemic inflammatory response accompanied by a pro-coagulant state and organ damage, particularly microvascular thrombi in the lungs and kidneys. Pathologic studies report strong evidence of complement activation. C5 blockade reduces inflammatory cytokines and their manifestations in animal studies, and has shown benefits in patients with aHUS, prompting investigation of this approach in the treatment of COVID-19. This review describes the role of the complement pathway and particularly C5a and its aberrations in highly pathogenic virus infections, and therefore its potential as a therapeutic target in COVID-19
 

wastwater

Senior Member
Messages
1,271
Location
uk
Is this virally lowered complement c3 in the liver then and the rest follows
C3 seems to have lots of aliases
aHUS3 is one alias

https://www.genecards.org/cgi-bin/carddisp.pl?gene=CFI

ases for CFI Gene

  • GeneCards Symbol: CFI 2
  • Complement Factor I 2 3 4 5
  • C3b-INA 2 3 5
  • KAF 2 3 5
  • FI 2 3 5
  • IF 3 4 5
  • Konglutinogen-Activating Factor 2 3
  • C3B/C4B Inactivator 3 4
  • C3b-Inactivator 2 3
  • Complement Control Protein Factor I 3
  • Complement Factor I Heavy Chain 3
  • Light Chain Of Factor I 3
  • Complement Component I 3
  • I Factor (Complement) 2
  • EC 3.4.21.45 4
  • EC 3.4.21 48
  • ARMD13 3
  • C3BINA 3
  • AHUS3 3
 

SWAlexander

Senior Member
Messages
1,943
Fatal COVID-19 has been associated with a systemic inflammatory response accompanied by a pro-coagulant state and organ damage, particularly microvascular thrombi in the lungs and kidneys.
I appreciate your post. This is further confirmation for VWF and APS and the mutation I found in my DNA results. Blood tests confirmed. One however is not mentioned Encephalitis.
 

SWAlexander

Senior Member
Messages
1,943
Encephalitis? Many symptoms would match.
There are several causes, including viral infection, autoimmune inflammation, bacterial infection, insect bites and others.
https://www.mayoclinic.org/diseases-conditions/encephalitis/symptoms-causes/syc-20356136

Stanford researchers find signs of inflammation in brains of people who died of COVID-19
https://med.stanford.edu/news/all-n...in-brains-of-people-who-died-of-covid-19.html

My DNA result after sepsis 2016: Staph epidermidis and Peptostreptococcus, one colony Staph caprae, Corynebacterium species
1679501336978.png

Blood test confirmed iin 2022 VWF and APS .