Following attachment, Marburg virions undergo endocytosis mediated through a mechanism that currently remains undetermined. (Figure 7 ) [16, 62] Initial studies investigating caveolin-mediated endocytosis showed that depletion of host cell cholesterol reduced viral infectivity but presented no direct evidence of caveolae involvement [169] . In addition, studies examining the role of caveolae in EBOV endocytosis are conflicting [169, 170] . A major role for clathrin in MARV entry has also been proposed based upon the ability of chlorpromazine (an inhibitor of both clathrin-mediated endocytosis and macropinocytosis) as well as RNAi-knockdown of clathrin heavy chain to inhibit MARV GP-pseudotyped HIV-1 entry [171] . A caveat to these analyses of MARV endocytosis is that they were performed only in the context of MARV GP-pseudotyped retroviruses which lack the characteristic filamentous morphology and size of Marburg virions.