Enterovirus 71 (EV71) is one of the major causative agents of
hand, foot and mouth disease (HFMD). Occasionally, EV71
infection is associated with severe neurological diseases, such as acute
encephalitis,
acute flaccid paralysis and cardiopulmonary failure. Several molecules act as
cell surface receptors that stimulate EV71
infection, including
scavenger receptor B2 (SCARB2),
P-selectin glycoprotein ligand-1 (PSGL-1), sialylated
glycan,
heparan sulfate and
annexin II (Anx2). SCARB2 plays critical roles in attachment, viral entry and uncoating, and it can facilitate efficient EV71
infection. The three-dimensional structures of the mature EV71 virion, procapsid and empty capsid, as well as the exofacial domain of SCARB2, have been elucidated. This structural information has greatly increased our understanding of the early steps of EV71
infection. Furthermore, SCARB2 plays essential roles in the development of EV71 neurological disease in vivo. Adult mice are not susceptible to
infection by EV71, but transgenic mice that express human SCARB2 become susceptible to EV71
infection and develop similar neurological diseases to those found in humans. This mouse model facilitates the in vivo investigation of many issues related to EV71. PSGL-1, sialylated
glycan,
heparan sulfate and Anx2 are attachment receptors, which enhance
viral infection by retaining the virus on the cell surface. These molecules also contribute to
viral infection in vitro either by interacting with SCARB2 or independently of SCARB2. However, the cooperative effects of these receptors, and their contribution to EV71 pathogenicity in vivo, remain to be elucidated.