Previous studies from HIV and other simple retroviruses have suggested that the enhanced fusion activities of some retroviral Env truncations in the CT may be due to increased steady-state levels of Env expression on the cell surface [56, 57, 58, 59] . However, here we have found little evidence that suggests that this might be the case for XMRV (Fig. 3C ) -despite the highly conserved endocytosis motif, YXXh (Y = tyrosine, X = any amino acid, h = residue with hydrophobic side chain) present in the CT of XMRV Env (Fig. 3A) . Another commonly assumed mechanism is that truncation of the retroviral Env CT can somehow alter the conformation of Env ectodomain, resulting in a reduced association between SU and TM thereby promoting membrane fusion [60] . Indeed, we observed that all three truncation mutants with enhanced fusogenicities, i.e., CT624, CT613 and CT609, exhibited increased levels of SU shedding, which was in sharp contrast to that of wildtype Env and other mutants (CT635, CT608 and CT606) having minimal cell-cell fusion activity (Fig. 3B, Figs. 4 and 5) . Future studies will focus on how the CT of XMRV Env structurally modulates the Env fusion activation.