Expression of SV2B, which has been shown to be involved in the regulation of synaptic vesicle exocytosis [24], was more reduced at 48 h post infection than in the early stages of infection (Table 1), whereas expression of the phagosome-related integrin (ITGB3), which functions as an ECM receptor, and the serpins B3 and B4, which bind heparin, leading to inhibition of the lysosomal cysteine protease cathepsin L, was markedly increased. The gene discussed is SV2B; the disease is infection.