These differences in dIgA reactivity among measles-infected subjects can be explained by three underlying possibilities: (i) variability in antigen preparation between commercial and in-house VL ELISA plates; (ii) saturation or competition of binding sites in NP by IgM; and (iii) dIgA is made as part of an early transitory response against specific antigens in lysate, rather than against NP. The gene discussed is CD40LG; the disease is measles.