The major hypothesis is that infection triggers the overproduction of pro-inflammatory Th1 cytokines, such as tumour necrosis factor (TNF), interferon-γ (IFN-γ), lymphotoxin (LT) and interleukin-12 (IL-12), leading to the up-regulation of leucocyte adhesion molecules (intercellular adhesion molecule-1 ICAM-1, vascular cell adhesion molecule-1 VCAM-1) on the cerebral microvascular endothelium, sequestration of pRBC, endothelial alterations and vascular obstruction. This evidence concerns the gene VCAM1 and infection.