As will be shown, the cytotoxic amyloids produced following infection are susceptible to various protein denaturing treatments, although pulmonary endothelial cell generated oligomeric tau was relatively resistant to degradation by proteinase K. Moreover, evidence will be presented demonstrating that a cytoprotective regulator of Aβ, cystatin C, is also produced during these infections. This evidence concerns the gene CST3 and infection.