Despite enhanced fusogenicity of CT624 and CT613, we found that the infection efficiency of their pseudovirions were rather low compared to those of wildtype Env (Tables 1 and 2 ). One plausible explanation is that the incorporations of these truncations into the MoMLV and HIV-1 vectors might be reduced as compared to those of wildtype; however, based on our immunoblot analysis using an anti-FLAG antibody to detect the XMRV SU, we found no evidence to support this scenario (Fig. 7) . Alternatively, the reduced pseudoviral titers for the truncation mutants might result from their altered ability to bind to the viral receptor, XPR1. While we do not have direct evidence in support of this possibility, the apparent SU shedding induced by the CT truncations in the Env-expressing cells (Fig. 3B ) strongly suggests that conformational changes likely occurs in the ectodomain of the truncated Env, including their SU subunits. Indeed, prior studies from HIV and other retroviruses have demonstrated that CT truncation of retroviral Env can alter the Env receptor binding capability thus affect viral infection [60, 64] . In this regard, it would be interesting to explore the role of the CT of XMRV Env in the infectious virus system.