Data from: de-stabilizing innate immunity in Covid-19: effects of its own positive feedback and erratic viremia on the alternative pathway of complement

Complement provides powerful, fast responses in the human circulation to
SARS-CoV-2 (Covid-19 virus) infection of the lower respiratory tract.
Covid-19 effects were investigated in a revised human in silico Mass
Action model of Complement’s Alternative pathway (AP) responses. Bursts of
newly circulating virions increased the fission of Complement protein C3
into C3a and C3b via stimulation of the lectin pathway or inhibited
Complement factor H. Viral reproduction sub-models incorporated smoothly
exponential or step-wise exponential growth. Starting complement protein
concentrations were drawn randomly from published normal male or female
ranges and each infection model run for 10 days. C3 and factor B (FB)
syntheses driven by Lectin Pathway stimulation led to declining plasma C3
and increasing FB concentrations. The C3 convertase concentration, a
driver of viral elimination, could match viral growth over three orders of
magnitude but near-complete exhaustion of circulating C3 was more
prevalent with step-wise than with “smooth” increases in viral
stimulation. C3 exhaustion could be prolonged. Type 2 Diabetes and
hypertension led to greatly increased peak C3 convertase concentrations,
as did short-term variability of Covid-19 viremia, pulmonary capillary
clotting and secondary acidosis. Positive feedback in the Alternative
pathway greatly extends its response range at the expense of stability.