C3 and infection: Lastly, the upregulation of sbi may suggest that pre-existing pH1N1 infection in alveolar epithelial cells may indirectly facilitate a strong immune evasion response in MRSA through interaction of bacteria with secreted messengers or agonists from damaged epithelium resulting in the inhibition of antibody responses through the binding of IgG and C3, a novel immune evasion approach [49].