IGHA1 and influenza: Based on the observation of Dotz et al, acute removal of sialic acid from Gd-IgA1 HR, for example due to infection by neuraminidase-secreting viruses (such as influenza) or bacteria (such as pneumococci), could contribute to increased amounts of Gd-IgA1 in the circulation, leading to enhanced binding of autoantibodies and formation nephritogenic CIC.