Oncogenic Retrovirus from Spontaneous Murine Osteomas. I. Isolation and Biological Characterization

Abstract

SUMMARYSpontaneous osteomas in strain 101 mice, a strain which has a high incidence of benign bone tumours, harbour numerous C-type virus-like particles with pleomorphic characteristics. A cell-free extract from osteomas from two mice induced bone tumours, together with osteopetrosis and lymphomas, in newborn mice of the low incidence NMRI strain after a latent period of 12 to 15 months. When C3H embryo fibroblasts were infected with the osteoma extract, the resulting cell line produced virus (OA MuLVc) with a high titre. OA MuLV c was cloned by serial endpoint dilution and NIH 3T3 cells were productively infected. The resulting virus was named OA MuLVN. OA MuLV c and OA MuLVN also induced bone tumours, osteopetrosis and lymphomas 12 to 15 months after injection into newborn NMRI mice. The isolated virus showed typical characteristics of the murine retrovirus group. Fv-1 host range restriction assays classified the viruses as N-ecotropic and XC-positive. Tryptic p30 peptide analysis and RNase T1 fingerprint analysis of OA MuLVc and OA MuLVy indicated that OA MuLVc contains an Akv-like virus as well as additional components, whereas OA MuLVN is closely related to Akv, but not identical to it. Serological analysis of the envelope proteins using monoclonal antibodies also showed the virus to be similar, but not identical, to Akv virus.

Osteosarcomagenic doses of radium (224Ra) and infectious endogenous retroviruses enhance proliferation and osteogenic differentiation of skeletal tissue differentiating in vitro

“…Although virus infection was established by immunohistochemistry, we did not observe the outgrowth of tumors after irradiation and transplantation into syngeneic mice. These findings are consistent with the biological effects of replication-competent retroviruses on skeletal cells in vitro [15,31 ] and similar to those observed after infection of newborn mice [7,28,32]. They indicate a prolongation of the cells' viability and abrogation of senescence together with an induction of differentiation in retrovirus-infected cells and tissues [15,31].…”

Mutation of All Runx (AML1/Core) Sites in the Enhancer of T-Lymphomagenic SL3-3 Murine Leukemia Virus Unmasks a Significant Potential for Myeloid Leukemia Induction and Favors Enhancer Evolution toward Induction of Other Disease Patterns

“…The mice were observed for tumor development 5 days per week. Moribund animals were sacrificed by cervical dislocation and examined for gross pathological changes including enlargement of thymus, spleen, liver, and mesenteric and peripheral lymph nodes, as previously described in detail (59). Lymphomatous tissues were dissected, and samples were stored frozen and/or fixed in 4% paraformaldehyde for further analysis.…”

Two Point Mutations Produce Infectious Retrovirus Bearing a Green Fluorescent Protein-SU Fusion Protein

“…A chronically infected NIH 3T3 cell line was established by exposing naive cells to a replication-competent, wild-type ecotropic MoMLV stock called OA virus (11) and culturing for 5 weeks of virus spread. The chronically infected cells (NIH 3T3/OA) were then exposed to dilutions of GFP-SU Q227R D243Y pseudotype virus produced by transient transfection of H1BAG cells.…”