Furthermore, Londrigan et al. even reported DC-SIGN as an alternative receptor for influenza H1N1 entry [28] and Hillaire et al. reported that in the absence of sialic acids, human influenza A viruses can replicate in DC-SIGN expressing cells, indicating that efficiency of DC-SIGN mediated infection is dependent on the extent of glycosylation of the viral hemagglutinin [27]. The gene discussed is CD209; the disease is infection.