The CT of retrovirus Env plays various roles in the replication cycle, including entry and assembly; this has been mostly studied in HIV-1 [48] . Here, we wished to determine the ability of XMRV Env and CT truncation mutants to pseudotype the MoMLV retroviral and HIV-1 lentiviral vectors as well as its relationship to membrane fusion and cell entry. As shown in Table 2 , all the XMRV Env constructs (tagged with a FLAG sequence at the N- terminus) were able to pseudotype both types of vectors but with distinct efficiencies. The full length XMRV Env exhibited approximately 2610 4 infectious units per ml for both vectors ( Table 2 , and data not shown), similar to a recent report [49] . The titers of MoMLV retroviral pseudotypes harbouring CT635 or CT624 were slightly reduced as compared to that of the wildtype Env (,4-6 fold), whereas the other more severely truncated mutants exhibited a 2,3-log decrease in the infectious titer ( Table 2) . Similar patterns were also observed for the HIV-1 lentiviral pseudotypes (Table 2 ), but interestingly we found that CT635 consistently exhibited pronounced reductions in the lentiviral pseudoviral titers (,100 fold) as compared that of MoMLV retroviral pseudotypes (,6-fold). The generally reduced viral titers for the CT truncations cannot be fully explained by the enhanced SU shedding, at least for some of these mutants, but appeared to correlate with the differential levels of SU surface expression (Fig. 2C) . We also examined the incorporation efficiencies of these Envs into the MLV pseudovirions by Western blot using concentrated pseudoviral particles, and detected similar levels of SU for CT624, CT613, CT609 and the wildtype Env, as compared to CT635, CT608 and CT606 for which the SU incorporation efficiency was greatly reduced (Fig. 7) . We have attempted to detect the XMRV TM in viral producer cells and the viral particles using an antibody against the MoMLV TM but without success (a gift from Marc Johnson, data not shown). Nevertheless, the Env incorporation data based on the SU (Fig. 7 ) and the XMRV pseudotype titers shown in Table 2 correlated with the SU expression profiles shown in Figure 3C . We noticed that the titers of pseudoviral infection for CT624 and CT613 did not correlate with their enhanced Env fusogenicity based on the syncytia formation and cell-cell fusion assays, and this was particularly the case for CT613, which showed a strongly enhanced fusogenicity (Figs. 4 and 5) but a much reduced titer relative to the wildtype Env (Tables 1 and 2 ).