As described for other GAG binding proteins, such as growth factors or chemokines36,37, the binding to the cell surface may potentially confer diverse advantages to the viral IFNα/βBP during infection, functioning as a retention and clustering mechanism to act mainly within infected areas, for protection against circulating plasma proteases or to allow interactions with other molecules, in addition to IFN-I. This evidence concerns the gene IFNA1 and infection.