The attachment and degradation of sialic acid residues by the neuraminidase (sialidase) of the influenza virus [20, 21], the direct infection of the endothelial cell by the influenza virus [22], or the release of inflammatory cytokines (TNF-α, IL-1β, and IL-6) that activate metalloproteinase can directly cleave proteoglycans, such as syndecan-1 [23]. The gene discussed is IL1B; the disease is infection.