XK and viral infectious disease: HA and NA interact with sialic acid receptors on the host cell surface, the former mediating membrane fusion that results in virus infection and the latter possessing sialidase activity that cleaves sialyl linkages between viral HA and cellular receptors to release progeny viruses and separate viruses from HA-mediated self-aggregation, allowing the virus to infect a new host cell for continuing virus replication [3].