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Increased antibody dependent complement deposition and lower antibody dependent phagocytosis has been observed in hospitalised COVID-19 patients associated with higher inflammation https://doi.org/10.1101/2021.01.11.426209 . This is intriguing as perhaps the type of antibody produced against SARS-CoV-2 has a role in promoting disease severity (via complement activation). This could also potentially involve auto-antibodies.

The association between complement activation and the biomarkers of endothelial damage suggests that complement may contribute to tissue injury and could be the target of specific therapy https://doi.org/10.1016/j.jaut.2020.102560

The complement of an event \(A\) in a sample space \(S\), denoted \(A^c\), is the collection of all outcomes in \(S\) that are not elements of the set \(A\). It corresponds to negating any description in words of the event \(A\).

The complement of an event \(A\) consists of all outcomes of the experiment that do not result in event \(A\).

Complement formula:

$$P(A^c)=1-P(A)$$

In contrast low C3 and C4 have been observed, though it is unclear whether this is decreased production or increased utilisation https://doi.org/10.21203/rs.3.rs-127493/v1

SARS-CoV-2 N protein is thought to bind MASP-2 as part of the lectin pathway.

The lectin pathway is thought to be generally increased in COVID-19 https://doi.org/10.1016/j.trsl.2020.11.008

L'autisme est un trouble neurodéveloppemental qui ne coupe pas de la réalité ni des relations, mais du sens (Harrison, Saint-Charles, 2018). Ici l'auteure définit brièvement l'autisme, elle généralise