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A clone of cells derived from a continuous line of cat cells (CCC) spontaneously produced an RNA C-type virus (CCC virus) which did not have the groupspecific antigen of the standard strains of feline leukemia viruses but did have that of the RD-114 virus. Single-hit infection of a virus yielding CCC cell with only the feline leukemia virus pseudotype of murine sarcoma virus [MSV(FeLV) ] resulted in the release of a pseudotype of MSV coated with the CCC virus envelope. Host range, transmission of virus, helper functions, interference properties, and specific neutralization showed that the CCC and the RD-114 isolates as well as their respective MSV pseudotypes are closely similar if not identical. Parental, virus-negative cells frozen before the existence of RD-114 were chemically induced to yield CCC-like virus de novo. Infection of susceptible human cells with the chemically induced virus resulted in interference with the CCC virus pseudotype of MSV but not with the FeLV pseudotype of MSV.

Small numbers of virus-like particles were observed by electron microscopy in each of two cloned lines of 3T3 cells transformed by murine sarcoma virus, even though these lines were free of detectable quantities of infectious leukemia and sarcoma virus. The morphology and occurrence of the particles were identical to those of the murine leukemia-sarcoma group. Moreover, the particles incorporated uridine and had a buoyant density of 1.16 g/ml in sucrose gradients. No evidence of sarcoma or leukemia virus infectivity was associated with the particles in cells of several susceptible species under various conditions, including both cosedimentation with leukemia virus and infection in the presence of inactivated Sendai virus. The particles may represent a form of murine sarcoma virus deficient' in one or more of the viral components necessary for infectivity.Several continuous lines of mouse embryo cells are susceptible to transformation and focus formation by murine sarcoma virus (MSV) (1, 2). Titration patterns of MSV in various isolates of mouse 3T3 cells indicate that focus formation in monolayer cultures under the usual assay conditions is dependent on dual infection by MSV and a murine leukemia virus (MuLV), which acts as a "helper" (1, 2). Thus, the behavior of MSV in mouse 3T3 cells, under certain culture conditions, is identical to that originally reported for MSV focus formation in mouse embryo cells (3). However, when culture methods are used that permit the multiplication of single transformed cells, while restricting reinfection of cells with progeny virus, both cell transformation and focus formation by MSV occur in the absence of MuLV "helper" virus and the properties of 3T3 cells infected with MSV alone can be examined (2,4).Growth of cells in semisolid agar suspension cultures is one such selective procedure that favors the multiplication of transformed cells and, at the same time, restricts virus spread (5). When 3T3 cells are infected with the Moloney isolate of MSV and plated as suspension cultures in semisolid agar, colonies of transformed cells can be seen after a suitable incubation period (2). The quantitative aspects of colony formation in this system indicate that cell transformation depends only on infection with MSV and occurs independently of infection with MuLV "helper" virus. Indeed, certain lines of MSV-transformed cells isolated from individual semisolid agar colonies contain a rescuable MSV genome in the absence of leukemia virus replication and have been designated "sarcoma-positive, leukemia-negative (S+L-)" (2). S+L-cells do not contain detectable quantities of focus-forming MSV unless superinfected with MuLV, after which both MSV and progeny MuLV are readily recovered (2). Transformation of mouse cells by MSV, therefore, does not require the replication of MuLV, and the "helper" activity of MuLV must involve either a quantitative or a qualitative effect on MSV replication.In addition to semisolid agar suspension cultures, monolayer cultures of 3T3 cells have also been us...

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Murine sarcoma virus transformed mouse 3T3 cells, which are negative for murine leukemia virus and which yield sarcoma virus after superinfection with murine leukenmia virus, spotaneously give rise to flat variants front which murine sarcoma virus can no longer be rescued. The revertants support leukemia viruis growth and show an enhanced sensitivity to murine sarcoma superinfection and, like normal cells, do not release RNA-dependent DNA polymerase activity. Because revertants could be obtained with high frequency from progeny of single transformed cells, each cell that containts the sarconma virus genome seems to have the capacity to suppress or eliminate an RNA tumor virus native to its species of origin.

A virus (M-7) isolated from baboon placental tissue demonstrates many similarities to endogenous feline virus RD-114. Immunodiffusion analysis shows a group-specific antigen (gs-1) line of identity between M-7 and RD-114. Anti-RD-114 DNA polymerase IgG inhibits M-7 polymerase by 57% compared to 97% for RD-114. M-7 virus has helper activity as demonstrated by rescue of murine sarcoma virus (MSV) from sarcoma-positive leukemia-negative human amnion cells. The host range of the rescued M-7 pseudotype of MSV, MSV (M-7), is similar to that of RD-114 virus. MSV (M-7) is also able to transform baboon cells and causes no detectable transformation of feline cells without addition of helper feline leukemia virus. Interference properties of M-7 and RD-114 virus are identical. Virus-specific neutralizing antisera, although partially cross-reacting, can distinguish MSV (M-7) from MSV (RD-114). These similarities and differences between RD-114 and M-7 viruses are best explained as type-specific differences between two viruses within the same strain. Recent electron microscope observations of C-type virus particles in normal baboon (Papio cynocephalus) placenta (15) led to their biochemical and immunological characterization (25). These data demonstrated that the particles had properties usually attributed to the C-type RNA tumor viruses, namely, common group-specific (gs) antigens and an RNAdirected DNA polymerase (25). Virus replication was found after the placental tissue was cocultivated with dog thymus cells (5); the virus isolated from these dog cells was designated M-7. Hybridization of the DNA transcript from M-7 virus RNA with baboon DNA suggested that it was an endogenous oncornavirus of the baboon (5). Ultrastructural studies of M-7 virus demonstrated, however, that the M-7 agent did not have the morphology of the human or subhuman placental particles (A. J. Dalton et al., J. Nat. Cancer Inst., in press) but closely resembled the C-type RNA tumor viruses of mouse, cat, and other primates. This paper will deal with biological and immunological characterization of the M-7 virus and will demonstrate certain striking similarities of this agent to the feline virus RD-114. MATERIALS AND METHODS Cell and culture techniques. Mouse 3T3FL, rat NRK, human F-49-1 amnion cell lines, and fifth 133