MARV GP mediates both cell attachment and fusion of the virus. There is convincing evidence that initial virus attachment at the cell surface can occur via the binding of GP carbohydrates to various cellular C-type lectins, including the hepatocyte-specific ASGP-R [87] , DC-SIGN and DC-SIGNR (also known as L-SIGN) [89, 92, 166] , hMGL [91, 92] , and LSECtin [166, 167] . Other cell surface proteins have also been implicated in facilitating MARV entry including the TAM receptor protein kinases Ax1, Dtk, and Mer [90] , and TIM-1 [93] . However, although these proteins may play a role in attachment or entry of certain cell types, the ability of MARV to infect cells lacking these receptors [92, 93, 168] indicates that there might be redundancy in cellular molecules required for MARV attachment to cells.