Studies examining the roles of endosomal proteases on the entry of MARV and EBOV have produced mixed results. Experiments analyzing recombinant VSV expressing EBOV GP indicate a primary role for Cathepsin B (CatB) and minor role for Cathepsin L (CatL) [181] . Entry of recombinant VSV particles containing MARV GP was inhibited when cells were treated with an inhibitor of both CatB and CatL [92] . These reports are confounded by a report conducted with infectious Marburg and Ebola viruses in which CatB and CatL inhibitors greatly reduced EBOV infection but showed mixed results with MARV [172] . Yet two other, more recent analyses determined that CatB was not required for MARV entry (although over-expression did enhance infectivity) and that CatL was required for entry into mouse embryonic fibroblasts but not Vero cells, 293T cells, or human macrophages [179, 180] . These data as well as the ability of other proteases to greatly diminish MARV infectivity [179, 180] , indicate that although CatB and CatL likely play a role in cleavage and activation of GP 1 in certain cell types, other endosomal proteases may also be able to facilitate GP 1 activation via cleavage.