Effect of mouse interferon on chemical carcinogenesis in normal rat kidney cells infected with Moloney murine leukemia virus.

The present study was carried out with a normal rat kidney cell clone that was initiated from a single cell infected by only one infectious particle of the non-transforming retrovirus, Moloney murine leukemia virus. Although the parental cells were highly resistant to chemical carcinogenesis, this infected clone was rendered susceptible to transformation by chemical carcinogens. However, when it was exposed to the tested carcinogen at a low subculture passage post-infection, cell transformation was detectable only after many subsequent passages.

Inhibition of retrovirus DNA supercoiling in interferon-treated cells.

The effect of interferon (IFN) on the cytoplasmic synthesis of murine sarcoma virus DNA, its transport to the host nucleus, and its integration into the cellular genome were investigated. For this purpose, at various intervals after infection. DNA was extracted from the cytoplasmic fraction, nuclear Hirt supernatant, and chromosomal DNA pellet.

The mechanism of interferon effect on cell transformation by murine sarcoma virus.

Mouse interferon (IFN) was found to inhibit murine sarcoma virus (MSV)-induced neoplastic transformation of normal rat kidney (NRK) cells. This effect was observed upon examining the formation of foci of morphologically altered cells and colonies of anchorage-independent cells. IFN had no cytotoxic effect on MSV-transformed NRK cells, nor on their focus or colony-forming ability.

Effect of mouse interferon on retrovirus production by chronically infected rat cells.

Mouse interferon (IFN) inhibited retrovirus release by both mouse and rat cells with the same efficiency. However, the antiviral state developed more slowly in rat than in mouse cells, and after removal of IFN it also persisted for a longer time in rat than in mouse cells. Under conditions where IFN strongly inhibited virus production it had no effect on cell replication nor on cellular RNA or protein synthesis.

Effect of mouse interferon on cell transformation and virus production in rat cells exogenously infected with moloney murine sarcoma and leukemia viruses.

Foci of transformed cells, produced by MSV(124), appeared to result only from the primary infection, since this virus stock yielded a virus-nonproducing infection. On the other hand, the majority of foci scored in MSV/MLV-infected cultures, were generated by multiple secondary infections with the progenies of the primary infection. Mouse interferon (IF) was highly inhibitory for cell transformation by both virus stocks.

Rapid purification of extracellular and intracellular Moloney murine leukemia virus.

The present study demonstrates the advantages of a combination of concentration by polyethylene glycol-6000 and Sepharose Cl-4B chromatography as a rapid procedure for retroviruses purification. This procedure can be completed within 3 hours, providing a high degree of virus purification with minimal damage to its structural and biological properties. Using transmission electron microscopy we observed many intracellular type-C virions in cytoplasmic vacuoles of 3T3/NIH cells chronically infected with Moloney murine leukemia virus.

Effect of interferon on assembly of intracellular Moloney murine leukemia virus particles in chronically infected 3T3/NIH cells.

The effect of interferon (IFN) on virus release and on assembly of intracellular virions in 3T3/NIH cells chronically infected with Moloney murine leukemia virus was studied by short labeling with 3H-leucine (viral proteins), 3H-glucosamine (viral glycoproteins) and 3H-uridine (vital RNA). With all of these labels, IFN pretreatment was found to strongly inhibit extracellular virus release. No difference was found between the extent of labeling of viral proteins and glycoproteins of intracellular virions.

Rapid syncytium formation induced by Moloney murine sarcoma virus in 3T3/NIH cells and its delay by mouse interferon.

Moloney murine sarcoma virus (MSV) clone 124 was found to induce rapid syncytium formation upon infection of 3T3/NIH at a high multiplicity of infection. This effect became apparent, by light microscopy, within 1 to 2 hours, whereas by scanning electron microscopy, clusters of 4 to 25 cells were seen in their initial steps of syncytium formation within 20 to 30 minutes after virus addition. It appeared that the cell fusion was initiated by connection between the cells through virus bound to their surface.