Submitted:
29 December 2025
Posted:
30 December 2025
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Abstract
Within Sudden Infant Death Syndrome (SIDS) resides several primary phenomena; these include a state of immune immaturity, susceptibility to infection, and an inflammatory state. Most SIDS risk factors pertain in some way or another to higher risk of infection (prematurity, lack of breastfeeding, low or absent transplacental antibody, ethnicity, genetics, risky gene polymorphisms, poverty, etc.). Most SIDS cases display evidence of an inflammatory state (raised inflammatory markers and inflammatory cytokines). The pattern of inflammation is very similar to that observed following vaccination, which for achieving successful levels of protective immunity requires components that induce high reactogenicity. It is this reactogenicity which, under certain circumstances can cause immune paralysis. Immune paralysis leaves a vulnerable infant open to infection and systemic inflammatory response syndrome leading to shock. Such a mechanism is explored in this rapid review in the context of the aetiopathogenesis of SIDS.

