Our observations suggest that during entry into BHK cells, BTV-1 is delivered to acidic compartments via a clathrin independent route. One possible route is uptake via caveolae as they can undergo fusion with early-endosomes [17] . However, the failure of DN-dynamin to inhibit BTV-1 entry and infection of BHK cells suggests that virus uptake is independent of caveolae. This conclusion was further supported by showing that BTV-1 infection was not inhibited by cholesterol depletion, which disrupts several lipid-raft dependent processes including caveolae-mediated endocytosis. Another clathrin-independent uptake route that leads to acidic endosomes is the CLIC/GEEC (CLathrin Independent Carriers/GPI-AP Enriched Endocytic Compartments) pathway [61, 62] . However, in contrast to the entry mechanism used by BTV-1 to infect BHK cells, the CLIC/GEEC pathway is highly sensitive to cholesterol depletion [62] and is, therefore, unlikely to mediate BTV-1 uptake. Recent studies have shown that vesicles derived from a number of other clathrin-independent pathways can fuse with early-or late-endosomes [22, 24, 63, 64] , and that viruses can use such mechanisms for infectious entry [15, 16, 24] . For example, Lymphocytic Choriomeningitis Virus (LCMV) and Kaposi's Sarcoma associated Herpesvirus (KSHV) are internalised by clathrin-independent mechanisms that result in virus delivery to late-endosomes without first passing through early-endosomes [65, 66, 67] . However, the uptake pathway used by LCMV appears distinct from that described here for BTV-1 entry into BHK cells in several ways including that LCMV uptake and infection are not blocked by inhibitors of macropinocytosis. The entry route used by KSHV appears more similar to that described here for BTV-1 since it also shares characteristics of macropinocytosis; however, unlike the BTV-1 BHK cell entry mechanism, entry of KSHV is not inhibited by dynasore and is therefore dynamin independent.