Sequence analysis of Mus dunni endogenous virus reveals a hybrid VL30/gibbon ape leukemia virus-like structure and a distinct envelope

Mus dunni endogenous virus (MDEV) is transcriptionally inactive in cultured M. dunni cells but can be activated by treatment of the cells with either hydrocortisone or 5-iodo-2′-deoxyuridine (24). Activation can be easily measured because MDEV can package Moloney murine leukemia virus (Mo-MLV)-based retrovirus vectors. Once activated, MDEV will continue to replicate in M. dunni cells and can infect many other cell types (4). MDEV is endogenous to M. dunni wild mice (also known as Mus terricolor) at a proviral copy number of one to two per genome, and there is at least one other element in dunni cells that hybridizes to MDEV probes, but it has a different restriction map (4). MDEV has not been found in the genomes of laboratory mice or in mammalian genera other than Mus (4). It is unknown whether MDEV causes pathology or is ever activated in M. dunni mice. MDEV does not interfere with known MLVs, indicating that it uses a different receptor for cell entry (26). MDEV also does not interfere with some nonmurine retroviruses, such as gibbon ape leukemia virus (GALV) (4). The endogenous cat retrovirus RD114 was found to interfere at a low level with MDEV, but this interference was observed in only one cell line (G355 cat glial cells) (4). Furthermore, this interference was weak and varied from one experiment to another, making it unclear whether MDEV and RD114 share a receptor in G355 cells. Other members of the RD114 interference group, such as spleen necrosis virus and Mason-Pfizer monkey virus, have not been found to interfere with MDEV (4). The MDEV receptor is widely expressed among different species, as indicated by the ability of a retroviral vector pseudotyped by MDEV to transduce cells from many species (4). Molecular clones of MDEV were obtained to study its genome and receptor usage (4). However, the clones were unable to produce infectious virus after transfection into permissive cells. Here we describe the correction of a clone that renders it infectious and show that the resulting virus is in the same interference group as the biological isolates. In addition, we have determined the entire sequence of MDEV and describe some unique features of the MDEV genome.