ART4 and influenza: Such conflicting data can be reconciled by recent results showing that α2,6-N-acetyl sialic-acid residues, known to interact with high affinity with human influenza HA [16], are expressed at high levels on all human B lymphocytes, independently of their activation status, either as intrinsic component surface-expressed glycoproteins, or bound to the lectin domain of B-cell-restricted CD22 inhibitory receptors [23].