Hepatocytes, endothelial cells, dendritic cells, monocytes, and macrophages, all of which express C-type lectins, are thought to be the preferred target cells of filoviruses Geisbert and Hensley, 2004; Hoenen et al., 2006) . Indeed, primary macrophage and dendritic cell cultures transduced for C-type lectin expression greatly increased their susceptibility to virus infection (Simmons et al., 2003a; Marzi et al., 2007) . While C-type lectins do not directly mediate filovirus entry, their pattern of expression in vivo and their ability to enhance infection indicate that C-type lectins can play an important role in filovirus transmission and tissue tropism. Thus, increased infection of these cells might be directly involved in the pathogenesis of filoviruses. Accordingly, it was shown that soluble mannose-binding C-type lectin played a role in protection from lethal Ebola virus infection in a mouse model (Michelow et al., 2011) . It should be noted that the ability to utilize the C-type lectins (i.e., DC-SIGN and hMGL) to promote cellular entry was correlated with the different pathogenicities among filoviruses (Takada et al., 2004; Marzi et al., 2006; Matsuno et al., 2010a) . Interestingly, the MLR amino acid sequence does not seem to be the primary factor contributing to the difference (Marzi et al., 2006; Matsuno et al., 2010a; Usami et al., 2011) . Although there might be some distinct mechanisms of entry between MARV and EBOV (Chan et al., 2000) , the similarity of tissue tropism and pathological features of infection between these viruses suggests that C-type lectins are one of www.frontiersin.org the important molecules, likely as attachment factors, for filovirus entry into cells, and that they are directly involved in filovirus tropism at the cellular level.