All CHO cell lines, including the latter, remained equally permissive to retroviral infection mediated by the VSV-G Env which enter cells through a different receptor, indicating that all cell lines had similar abilities to support general retroviral infection past viral entry (Fig. 3d), and that defects in infection by the p.(L612_696Tdel) construct was solely due to the absence of this artificial mutant at the cell surface. This evidence concerns the gene ERVW-1 and infection.