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P T Peebles

Publications and source records attributed to P T Peebles.

At least 19 recordsLinked to original sources
PubMed1978

Further evidence for deletion of envelope glycoprotein (gp69/71) sequences in formation of Moloney-murine sarcoma virus.

Moloney-murine sarcoma virus (S+L- strain of M-MSV) has been nonproductively cloned in murine and non-murine host cells (S+L- cells) and the expression of Moloney leukaemia virus (M-MuLV) 30000 mol. wt. core protein (p30) and envelope glycoprotein (gp69/71) were studied by radioimmunoassay. Antigenic determinants of the M-MuLV p30 were associated with the sarcoma virus genome in these non-productively transformed cell clones studied, while the determinants of M-MuLV gp69/71 were not. The absence of envelope-associated glycoprotein expression in sarcoma virus transformed cells was confirmation of biological studies demonstrating that rescued sarcoma virions acquire envelope-associated properties of host range, neutralization and interference from rescuing helper virus, and further evidence that the M-MuLV gp69/71 sequences have been deleted during the formation of the M-MSV. During the course of these studies, it was also found that S+L- dog cells were releasing into culture supernatant large amounts of the p30 antigenic determinant, apparently as a soluble antigen.

Cell Line↗
PubMed1976

Increased sarcoma virus RNA in cells transformed by leukemia viruses: model for leukemogenesis.

A morphologically flat revertant of mink cells nonproductively infected with Moloney sarcoma virus exhibited contact inhibition and lacked detectable sarcoma virus RNA. Superinfection by usually nontransforming type C mammalian leukemia-causing viruses induced transformation and increased sarcoma virus RNA. The results suggest a model for leukemogenesis in animals by increasing, during replication of usually nontransforming leukemia viruses, the levels of RNA from potentially oncogenic cell or integrated virus transforming genes.

Cell Transformation, Neoplastic↗
PubMed1975

Two active forms of RD-114 virus DNA polymerase in infected cells.

Two forms of DNA polymerase are present in RD-114-infected human, dog, and mink cells, but are not detectable in uninfected cells. The two enzymes are indistinguishable catalytically and immunologically, but differ with respect to molecular weight and elution position from (dT)12-18-cellulose and phosphocellulose. The large enzyme (equivalent 95,000 daltons) is found in the infected cells, but not the virions produced by these cells. The virions contain only the smaller enzyme (equivalent 70,000 daltons). The larger form may represent a mammalian viral equivalent to the beta subunit of avian RNA tumor virus DNA polymerase.

Cell Line↗
PubMed1975

Separation of sarcoma virus-specific and leukemia virus-specific genetic sequences of Moloney sarcoma virus.

We have studied the nucleic acid sequences in nonproducer cells transformed by Moloney sarcoma virus or Abelson leukemia virus (two types of replication-defective, RNA-containing, viruses isolated by passage of Moloney leukemia virus in BALB/c mice). DNA probes from the Moloney leukemia in virus detect RNA in both Abelson virus-transformed nonproducer cells and Moloney sarcoma virus-transformed nonproducer cells. A sarcoma-specific cDNA, prepared from the Moloney sarcoma virus, has extensive homology to RNA found in heterologous nonproducer cells transformed by Moloney sarcoma virus, has little homology to RNA in cells producing Moloney leukemia virus, and no detectable homology to RNA in nonproducer cells transformed by the Abelson virus. By analogy to earlier data on avian and mammalian sarcoma viruses, these results suggest that the Moloney sarcoma virus arose by recombination between a portion of the Moloney leukemia virus genome and additional sarcoma-specific information, and indicate that the expression of this information in not essential for Abelson virus-mediated fibroblast transformation.

Cell Line↗
PubMed1975

Human amnion and lung tissue culture systems for possible detection and study of human RNA tumor viruses.

A human lung and an amnion cell line were identified as highly susceptible to transformation by the rhabdomyosarcoma-114 (RD-114) virus pseudotype of murine sarcoma virus (MSV). MSV transformation on these two cell lines demonstrated a) "one-hit" kinetics with an MSV stock which contained a 100-fold excess of MSV over its detectable associate RD-114 helper virus and b) only a slight increase (2X) in focus-forming titers by the addition of optimal concentrations of RD-114 helper virus. These findings indicated that the primary MSV interaction with those amnion and lung cells was that of non-productive transformation; and this was confirmed by the isolation of sarcoma-positive leukemia (helper) virus-negative (S+Lminus) cells from cloned terminal foci of MSV transformed human amnion and lung cells. These MSV-susceptible human cell lines are the first human cells identified as capable of demonstrating the defective nature of MSV. Human candidate oncornaviruses have not, however, been detected to date with the use of normal lung and amnion cells and their S+Lminus derivatives as indicator systems. These cell lines were useful for the isolation and identification of a new RD-114-like virus from a cat cell line.

Amnion↗
PubMed1975

Control of reversion of Moloney virus sarcoma virus transformed cells.

Mouse cells transformed by the Moloney murine sarcoma virus (MSV) native to the species can give rise to revertants which are supersusceptible to a second cycle of transformation. The MSV retransformed cells can give rise to several complex functional states even after several cycles of cloning: a) Formation of sarcoma positive, leukemia negative (S+Lminus) type cells of which some sublines may be inducible for MSV by halogenated pyrimidines; b) detection of initially SminusLminus cells which spontaneously become transformed and S+Lminus; c) the derivation of flat murine leukemia virus positive (MuLV+) cells which have an atypical MuLV and may become MSV+ as well as MuLV+; d) the release of free MSV from some cell clones with an apparent absence of MuLV. A general feature of all the above variants is a failure of detection of spontaneous reversion occurring after the second cycle of transformation. The nature of MuLV spontaneously released is that of a poorly replicating MuLV which exhibits cross-interference with other MuLV pseudotypes of MSV and the envelope which is most similar to that of Moloney leukemia virus (MLV). The examination for spontaneous reversion in human S+Lminus cells transformed by the same type of genome capable of good frequency of reversion in mouse cells, did not yield human revertant cells.

Cell Transformation, Neoplastic↗
PubMed1974

Baboon virus isolate M-7 with properties similar to feline virus RD-114.

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.

Amnion↗
PubMed1973

Isolation of RD-114-like oncornavirus from a cat cell line.

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 group-specific 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.

Animals↗
PubMed1972

Reversion of murine sarcoma virus transformed mouse cells: variants without a rescuable sarcoma virus.

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.

Animals↗
PubMed1972

Deficiency of viral ribonucleic acid-dependent deoxyribonucleic acid polymerase in noninfectious virus-like particles released from murine sarcoma virus-transformed hamster cells.

Virions from hamster cells transformed by a new strain of murine sarcoma virus (MSV) appear to represent a form of MSV deficient in one or more of the viral components necessary for infectivity. Both the noninfectious virions and the sarcoma virus-transformed cells, which have no detectable replicating leukemia helper virus of either murine or hamster origin, are deficient in viral-type ribonucleic acid (RNA)-dependent deoxyribonucleic acid (DNA) polymerase activity (i.e., reverse transcriptase activity stimulated by the synthetic RNA-DNA template polyribo-adenylic-oligodeoxythymidylic acid). In comparison, both murine leukemia virus (MuLV) and MuLV-infected cells have abundant viral-type reverse transcriptase activity. It appears, therefore, that the leukemia virus genome may be required for the production of infectious sarcoma virus by contributing information needed for the full expression of functional viral-type reverse transcriptase.

Animals↗