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At least 19 recordsLinked to original sources
PubMed1984

Heteroduplex analysis of molecular clones of the pathogenic Friend virus complex: Friend murine leukemia virus, Friend mink cell focus-forming virus, and the polycythemia- and anemia-inducing strains of Friend spleen focus-forming virus.

The pathogenic Friend virus complex is of considerable interest in that, although members of this group are genetically related, they differ markedly in biochemical and biological properties. Heteroduplex mapping of molecular clones of the Friend virus complex, which includes the replication-competent ecotropic Friend murine leukemia virus (F-MuLV) and mink cell focus-forming virus (F-MCF) and replication-defective polycythemia- and anemia-inducing strains of spleen focus-forming virus (SFFVp and SFFVa, respectively), was employed to provide insight into the molecular basis of their relationships. In heteroduplexes of F-MuLV X F-MCF, a major substitution of 0.89 kilobases in the env gene of F-MCF was discerned. Heteroduplexes of SFFVp X F-MuLV or F-MCF and SFFVa X F-MuLV or F-MCF showed several major deletions in the pol gene region and a single major deletion in the 3' half of the env gene region of SFFVp and SFFVa. A major substitution of 0.89 kilobases was mapped to the 5' end of the env deletion of SFFVp and SFFVa in heteroduplexes with F-MuLV, similar to that seen in F-MuLV X F-MCF heteroduplexes. In contrast, this env gene region was totally homologous in F-MCF X SFFVp or SFFVa and SFFVp X SFFVa heteroduplexes. Our results suggest that (i) both SFFVp and SFFVa lack part of the env gene at its 3' end, corresponding to the p15(E) coding region, (ii) major deletions occur in the pol and env genes which account for the replication defectiveness of SFFVp and SFFVa, (iii) minor substitutions occur in the gag gene region of SFFVa that are not present in SFFVp, F-MuLV, or F-MCF, (iv) a major substitution exists in the gp70 region of the env gene between F-MuLV and F-MCF that probably accounts for the differences in their host range specificities, (v) this substitution in F-MCF is identical to the gp70 part of the gp52 coding region of SFFVp and SFFVa, and (vi) heteroduplexes to F-MCF show unambiguously that no additional large substitutions are present in SFFVp or SFFVa that could account for differences in their leukemogenicity.

Animals↗
PubMed1995

[Preschoolers' understanding of characteristics of their friends' behavior: prediction of friends' behavior and behavioral intention toward friends].

These studies examined preschoolers' understanding of characteristics of friends. "Friends" were defined as children of the same sex who chose each other as good friends, and "acquaintances" were those who knew each other but did not mutually chosen. In Study 1, 30 five- to six-year-old children were asked how they expected their friends and acquaintances to behave toward them in various situations, such as play, help, and trust situations. It was found that they tended to expect their friends in play and trust situations to behave more kindly than their acquaintances. In Study 2, they were asked how they themselves would behave toward their friends and acquaintances in the same situations. They replied that they would behave more kindly toward their friends than toward their acquaintances in all the situations. These results were interpreted as preschoolers showing a consistent understanding of their friends' behavior, as well as a clear comprehension of reciprocity in their relationship with their friends.

Child↗
PubMed1981

New cell surface gp70 related to Friend mink cell focus-inducing virus is expressed on Friend virus-induced erythroleukemic spleen cells after elimination of ecotropic Friend virus gp70 in Rfv-3r/s mice.

Spleen cells from Rfv-3r/s mice with Friend virus-induced erythroleukemia were analyzed for expression of virus-induced proteins with monoclonal antiviral antibodies and conventional antisera. Leukemic spleen cells, 30-60 d after virus inoculation, expressed decreased amounts of ecotropic Friend murine leukemia helper virus gag- and env-encoded cell surface and intracellular proteins compared with leukemic cells tested 8-10 d after virus inoculation. In contrast, the spleen focus-forming virus-induced protein, gp55, was present on both leukemia cell populations. This difference appeared to be mediated by the humoral antibody response in Rfv-3r/s mice, which could recognize only ecotropic gag and env proteins, and not gp55. A new gp70 molecule cross-reactive with a recombinant Friend mink cell focus-inducing virus was found in large quantities on late leukemic cells. This protein appeared to be derived from a recombinant virus produced during the course of Friend virus infection. The appearance of this new gp70 suggests that recombinant viruses other than spleen focus-forming virus may play a role in Friend virus-induced erythroleukemia.

Animals↗
PubMed1973

Resistance of mice to infection with Friend disease virus after subcutaneous injection of Friend virus and Friend spleen cells.

Swiss mice injected subcutaneously with suspensions of spleen cells or an extract of spleens from mice infected with Friend virus develop resistance to subsequent intravenous inoculation of Friend virus. A single injection of either Friend virus or Friend cells induces resistance. Immunized mice display resistance when challenged 6 months after immunization and survive for at least 20 weeks after infection. Neutralization tests indicate that serum, but not lymphoid cells of resistant animals, can neutralize Friend virus. In vitro neutralization tests indicate that residence of virus within the peritoneal cavity of immune mice for 1 h sharply reduces the infective titer of the virus.

Animals↗
PubMed1990

Having friends, keeping friends, making friends, and being liked by peers in the classroom: predictors of children's early school adjustment?

The potential role that children's classroom peer relations play in their school adjustment was investigated during the first 2 months of kindergarten and the remainder of the school year. Measures of 125 children's classroom peer relationships were obtained on 3 occasions: at school entrance, after 2 months of school, and at the end of the school year. Measures of school adjustment, including children's school perceptions, anxiety, avoidance, and performance, were obtained during the second and third assessment occasions. After controlling mental age, sex, and preschool experience, measures of children's classroom peer relationships were used to forecast later school adjustment. Results indicated that children with a larger number of classroom friends during school entrance developed more favorable school perceptions by the second month, and those who maintained these relationships liked school better as the year progressed. Making new friends in the classroom was associated with gains in school performance, and early peer rejection forecasted less favorable school perceptions, higher levels of school avoidance, and lower performance levels over the school year.

Achievement↗
PubMed1989

RB virus: a strain of Friend virus that produces a 'Friend virus-like' disease in Fv-2rr mice.

RB virus is a newly derived strain of Friend virus that was adapted to produce a 'Friend-like' disease in mice that are genetically resistant to wild-type Friend virus. RB virus was produced by passing high titers of the wild-type Friend virus (Lilly-Steeves polycythemia-producing strain) through adult Fv-2rr mice. Titration of the defective spleen focus-forming virus indicated RB virus infected similar numbers of Fv-2ss or Fv-2rr target cells. Analysis of the spleens from mice infected with RB virus indicated that RB induced the early stage of Friend disease (erythroid proliferation) in both Fv-2rr and Fv-2ss mice. Fv-2ss mice infected with RB virus developed the classical Friend disease within 3 weeks. In contrast, the percentage of Fv-2rr mice developing the 'Friend-like' disease after infection with RB virus never exceeded 60%. The latency period of RBV in Fv-2rr mice was strain dependent. D2.R16 (Fv-2rr) developed the syndrome more rapidly than C57BL/6 (Fv-2rr). RB virus retained the capacity to transform erythroprogenitor cells from both Fv-2ss and Fv-2rr animals. Cells infected with RB virus consistently produced a modified SFFV envelope protein, gp48.

Animals↗
PubMed1980

Studies of cloned Friend erythroleukemia tumor cells. Modulation of the tumor-specific cytologic T lymphocyte response by infectious Friend virus production in vitro.

The HFL/b tumor cell line, induced by Friend erythroleukemia virus in BALB.B mice, was used to study the relation between virus production or nonproduction and the antigens recognized by Friend virus-specific cytolytic T lymphocytes (CTL). Analysis of clones and subclones of these tumor cells revealed a high degree of heterogeneity with respect to the production and release into culture fluids of infectious Friend virus in vitro, ranging from high levels to low or undetectable levels of virus production. Although no major differences could be detected among the antibody-defined serotypes of the various clones, the susceptibility of cells of individual HFL/b clones to attack by Friend virus-specific CTL varied widely, and those clones which produced large amounts of infectious virus provided the most sensitive target cells. It was also apparent that production of infectious Friend virus was inhibitory to CTL generation in syngeneic mixed leukocyte-tumor cell cultures. Friend erythroleukemia virus-producing cells thus appeared to interact in a complex manner with the host CTL response by modulating their production of infectious Friend virus.

Animals↗
PubMed1984

Leukemia induction by a new strain of Friend mink cell focus-inducing virus: synergistic effect of Friend ecotropic murine leukemia virus.

A new strain of Friend recombinant mink cell focus-inducing retrovirus, FMCF -1-E, was found to induce leukemias in NFS and IRW mice. Although the isolate was obtained from a stock of FMCF -1 ( Troxler et al., J. Exp. Med. 148:639-653, 1978), FMCF -1-E was distinguishable from FMCF -1 by oligonucleotide fingerprinting and antigenic analysis, using monoclonal antibodies. These analyses suggested that FMCF -1-E is a distinct FMCF isolate rather than a simple variant of FMCF -1. After neonatal inoculation, the latency for leukemia induction was 3 to 8 months. A similar long latency was also seen when Friend murine leukemia virus 57 was inoculated into adult (6-week-old) IRW mice. However, sequential inoculation of FMCF -1-E at birth followed by Friend murine leukemia 57 at 6 weeks of age led to a shortened latency period (2.5 to 4 months). Only neonatal inoculation of Friend murine leukemia virus 57 was able to induce a more rapid appearance of leukemia. The leukemia cell type in the majority of cases, regardless of virus inoculation protocol, was erythroid, but occasional myeloid, lymphoid, and mixed leukemias were also observed. In contrast to NFS and IRW mice, BALB/c mice were resistant to leukemia induction by FMCF -1-E and also showed some transient resistance to leukemia induction by Friend murine leukemia virus 57.

Animals↗
PubMed1991

Conversion of Friend mink cell focus-forming virus to Friend spleen focus-forming virus by modification of the 3' half of the env gene.

The 3' half of the env gene of the dualtropic Friend mink cell focus-forming virus was modified by replacing the restriction enzyme fragment of the genome DNA with the corresponding fragment of the acutely leukemogenic, polycythemia-inducing strain of Friend spleen focus-forming virus (F-SFFVP) genome DNA. Replacement with the fragment of F-SFFVP env containing the 585-bp deletion, the 6-bp duplication, and the single-base insertion converted the resulting chimeric genome so that the mutant had a pathogenic activity like that of F-SFFVP. Replacement with the fragment containing only the 585-bp deletion did not result in a pathogenic virus. However, when this virus pseudotyped by Friend murine leukemia virus was passaged in newborn DBA/2 mice, we could recover weakly pathogenic viruses with a high frequency. Molecular analysis of the genome of the recovered virus revealed the presence of a single-base insertion in the same T5 stretch where the wild-type F-SFFV env has the single-base insertion. These results provided evidence that the unique genomic structures present in the 3' half of F-SFFV env are the sole determinants that distinguish the pathogenicity of F-SFFV from that of Friend mink cell focus-forming virus. The importance of the dualtropic env-specific sequence present in the 5' half of F-SFFV env for the pathogenic activity was evaluated by constructing a mutant F-SFFV genome in which this sequence was replaced by the ecotropic env sequence of Friend murine leukemia virus and by examining its pathogenicity. The results indicated that the dualtropic env-specific sequence was essential to pathogenic activity.

Animals↗
PubMed1985

Induction of the early stages of Friend erythroleukemia with helper-free Friend spleen focus-forming virus.

The polycythemia-inducing strain of Friend virus (FV-P) causes a multistage erythroleukemia in susceptible mice. FV-P is a complex of two viruses, a replication-competent virus [Friend murine leukemia virus (F-MuLV)] and a replication-defective spleen focus-forming virus (SFFVp). We have addressed directly the role of SFFVp in the induction of the early stages of Friend disease by constructing stocks of SFFVp free of detectable F-MuLV, using a recently described retroviral helper-cell line. These preparations are capable of inducing erythroid bursts (vBFU-E) whose inducibility, kinetics, and responsiveness to erythropoietin suggest that they are very similar, if not identical, to the vBFU-E induced by FV-P. Single injections of helper-free SFFVp had no apparent effects in vivo, although the addition of exogenous helper virus to the inoculum resulted in the induction of classic Friend disease. Increasing the effective titer by giving mice five daily virus injections resulted in the induction of splenomegaly and a large increase in the number of erythroid colony-forming units that were independent of erythropoietin. When the injections were discontinued, the spleens regressed and all the mice survived. When the injections were continued, all the mice died within 25 days of the first injection. These results demonstrate that SFFVp alone can alter the growth characteristics of erythroid progenitors and is directly responsible for the induction of vBFU-E in vitro and the erythroid hyperplasia in vivo. They also demonstrate that the initial polyclonal stage of Friend disease is reversible and can be reproduced by using preparations of SFFVp free of detectable F-MuLV.

Animals↗
PubMed1986

Friend murine leukemia virus and spleen focus-forming virus expression in highly malignant interferon-sensitive and interferon-resistant Friend leukemia cells.

Analysis of expression of the Friend murine leukemia virus (F-MuLV) and of the spleen focus forming virus (SFFV) has been undertaken in highly malignant interferon (IFN)-sensitive (745) and IFN-resistant (3Cl-8) Friend leukemia cells (FLC), serially passaged intraperitoneally in DBA/2 mice. In vivo passaged 745 cells, as well as the clones derived thereof, did not release Friend virus (FV). Western blot analysis of the plasma membrane fractions of the virus nonproducer 745 cells revealed the lack of gp69/70 glycoprotein expression. At least 10 intraperitoneal passages of virus producer in vitro passaged of virus producer in vitro passaged 745 cells were necessary to obtain the selection of the virus nonproducer phenotype. In contrast in vivo passaged 3Cl-8 cells continued to produce FV even after 100 in vivo passages and expressed gp69/70 antigens to a similar extent as the original in vitro passaged FLC. The expression of F-MuLV and SFFV RNAs in virus producer and virus nonproducer FLC clones has been investigated by means of Northern blot technique using probes specific for either F-MuLV or SFFV. No F-MuLV specific RNA sequences were detected in virus nonproducer 745 clones. SFFV specific RNA transcripts and gp52/55 glycoprotein production could be revealed in all the FLC tested. Southern blot analysis showed the presence of F-MuLV specific sequences in the cellular DNA of virus nonproducer 745 clones. As both in vivo passaged F-MuLV producer 3Cl-8 and F-MuLV nonproducer 745 cells were equally barely immunogenic and highly malignant when injected into syngeneic DBA/2 mice, these results indicate that F-MuLV expression does not result per se in a high immunogenic potential of tumor cells. For the time being, as a specific property of 3Cl-8 versus 745 cells is the interferon-resistant phenotype, it is tempting to speculate that the selection of virus nonproducer cell variants after in vivo passages of interferon-sensitive 745 cells could depend on the presence of low levels of endogenous interferon in normal young mice.

Animals↗
PubMed1983

Expression of Friend leukemia virus and spleen focus-forming virus-specific sequences in erythroid bursts and granulocyte-macrophage colonies from spleen and marrow of mice infected with Friend leukemia virus.

A large number of studies have been carried out to identify the Friend leukemia virus (FV) target cell(s). In FV-infected mice, the kinetics of "primitive" erythroid burst-forming units (P-BFU-E) is perturbed, and their proliferative rate is enhanced. These results indirectly suggest, but do not prove, that cycling P-BFU-E may serve as FV target. In vitro infection studies showed that normal erythroid colony forming units (CFU-E) and "mature" erythroid burst-forming units (M-BFU-E) are targets for FV, while the largely out-of-cycle normal P-BFU-E are not. In an attempt to shed light on these aspects, we have evaluated the expression of viral cytoplasmic RNA sequences in pools of colonies generated by P-BFU-E and granulocyte-macrophage colony forming units (CFU-GM) from spleen and marrow of polycythemic Friend virus (FVP)-infected mice, as measured by liquid hybridization with FVP- or spleen focus-forming polycythemic virus (SFFVp)-specific DNA probes. Moreover, similar assays were performed on RNAs derived from whole spleen or bone marrow from mice treated with FVP or the anemic strain of Friend virus (FVA). Control studies were performed on corresponding colonies and whole tissues from normal animals. FVP- and SFFVp-specific sequences are more abundant in RNA extracted from infected spleen as compared to marrow by a 10-fold factor. On the other hand, FVP and SFFVp-specific sequences are expressed at a comparable level in both P-BFU-E- and CFU-GM-derived colonies from spleen or marrow of FVP-treated mice. Since in vitro spread of FVP infection was excluded by control studies with addition in culture of antibody to the viral glycoprotein with a molecular weight of 70,000 (gp70) these results indicate that P-BFU-E and CFU-GM are infected in vivo by FVP.

Animals↗
PubMed1984

Lysis of FLD-3 Friend erythroleukemia cells in vitro and in vivo: effect of 89Sr treatment and Friend virus infection.

The effector cells from non-immunized mice capable of lysing 51Cr-labelled FLD-3 BALB/c Friend virus-induced erythroleukemia cells in vitro and cells capable of clearing FLD-3 cells labelled with 5-iodo-2'-deoxyuridine-125I (125IdUrd) from the lungs in vivo were characterized and compared with natural killer (NK) cells reactive against YAC-I lymphoma cells. Unlike NK cells, the cells capable of lysing FLD-3 cells in vitro were insensitive to antibodies directed against NK-2.1 or Thy-1.2 antigens (plus complement) and to pretreatment of mice in vivo with silica particles, 89Sr or estradiol. Heat-killed C. parvum organism stimulated anti-FLD-3 effector cells without changing the slow rate (24 h) of lysis in vitro. The ability to clear FLD-3 and YAC-1 cells from the lung was normal and defective, respectively, in C57BL/6-bg/bg(beige) mice and in mice pretreated with 89Sr or estradiol. We conclude that natural cytotoxic (NC) cells lyse FLD-3 cells, Fv-2, which regulates resistance to leukemia induction by Friend virus, does not regulate NC(FLD-3) activity, and the virus does not affect NC(FLD-3) activity during the first several days of infection of normal genetically susceptible mice. However, infection of 89Sr-treated mice inhibits NC(FLD-3) function owing to the activation of suppressor cells. These data suggest (but do not prove) that effector cells similar or identical to NC(FLD-3) cells may function in vivo to resist the proliferation/survival of certain leukemia cells.

Animals↗
PubMed1987

Reduced maturation of Friend virus in adhesive mutants of Friend leukemia cells.

The replication of Friend Leukemia virus (FLV) has been investigated in adhesive clones (FF) of Friend Leukemia cells which were selected via cultivation on top of human fibroblast monolayers. In these adhesive clones a shut-down of FLV production is observed under conditions of culture confluency; this finding is not due either to a reduced number of cell divisions nor to a defective expression of FLV genome as assessed by Northern blot and immunofluorescence studies. Ultrastructural studies showed that virus budding and release into the medium is not detectable under these conditions. Conversely, in confluent FF cell monolayers abundant imperfect type-A enveloped particles were visible, possibly originating from stacks of granular endoplasmic reticulum with thickened membranes. It is postulated that the reduced virus production in adhesive FF monolayers is due to as yet undetermined events taking place during virus maturation at a time coincident with that of cell-cell adhesion under conditions of culture confluency.

Animals↗
PubMed1983

Characterization of monoclonal antibodies reactive with murine leukemia viruses: use in analysis of strains of friend MCF and Friend ecotropic murine leukemia virus.

Sixteen mouse and rat monoclonal antibodies reactive with gag or env proteins of Friend murine leukemia virus (F-MuLV) or recombinant MCF viruses related to F-MuLV were derived. Specificity of these was determined by immunofluorescence, immunoprecipitation, and reactivity with viral proteins blotted onto nitrocellulose paper. Seven antibodies reacted with envelope protein antigens of certain nonecotropic viruses only. Nine antibodies reacted with both ecotropic and nonecotropic viruses. Of this latter group, three were antienvelope, four were anti-p15, one was anti-p12, and one was anti-p30 in specificity. When tested as a panel against 10 strains of F-MuLV, these antibodies could distinguish seven different antigenic patterns. However, all 10 strains retained reactivity for three anti-gp70 antibodies uniquely specific for Friend and Rauscher MuLVs. Our antibody panel could also identify MCF viruses isolated from mice neonatally inoculated with F-MuLV as recombinants related to a particular F-MuLV strain based on identity of p15 gag antigenic profiles. However, recombinant viruses lacked several envelope antigens always associated with F-MuLV and instead had new envelope reactivities. These anti-MCF monoclonal antibodies detected no shared envelope antigens between MCF and xenotropic viruses isolated from mice inoculated with F-MuLV, however many of them did react with MCF viruses derived from AKR mice and NFS mice congenic for endogenous ecotropic virus loci.

Animals↗
PubMed1991

Identification of an epitope encoded in the env gene of Friend murine leukemia virus recognized by anti-Friend virus cytotoxic T lymphocytes.

We have previously shown that strong epitopes recognized by anti-Friend virus (FV) cytotoxic T lymphocytes (CTL) in H-2b mice are encoded in both the env and gag/pol regions of the helper friend leukemia virus genome. Two approaches have been used to identify these epitopes. At the nucleic acid level, we have constructed env genes with either of two in-frame deletions: pKR2, an env gene with a 681-bp deletion in the gp70 region and inserted into the pSV2-gpt-1 expression vector; and pKR1, an env gene with an 81-bp deletion in the p15E region and inserted into pSV2-gpt-1. Cell clones were established by transfecting Fisher rat embryo cells with pDb (the H-2Db restriction element), pNEO (for G418 selection) and either pKR1 or pKR2. Db and env gene expression was monitored by immunoprecipitation with polyclonal antibodies or by detection of viral RNA on Northern blots. Expressor cell clones were tested for susceptibility to lysis by polyclonal anti-FV/Db CTL in 51Cr-release assays. Whereas cells expressing pKR1 were lysed to the same extent as cells expressing the intact env gene, cells expressing pKR2 were resistant to lysis, suggesting that all detectable env epitopes are encoded within the 681-bp deletion. Polypeptides representing the two most likely candidate epitopes encoded in this segment were synthesized and tested for their abilities to sensitize FRE cells expressing Db alone for lysis by the CTL. One 17-mer polypeptide, AGTGDRLLNLVQGAYQA [corrected], functioned as a strong CTL epitope in this assay, but the other 18-mer polypeptide was inactive. Studies of the role of this epitope in the immune response to candidate viral vaccines are in progress.

Amino Acid Sequence↗
PubMed1992

Approach to a retrovirus vaccine: immunization of mice against Friend virus disease with a replication-defective Friend murine leukemia virus.

In an initial attempt to test the ability of replication-defective retroviruses to immunize against immunologically related pathogenic viruses, we have worked with the erythroleukemogenic Friend retrovirus complex (FV), which consists of a replication-competent helper component, Friend murine leukemia virus (FMuLV), and a related defective pathogenic component, spleen focus-forming virus (SFFV). An 81-base-pair deletion was introduced into the p15E-encoding region of the env gene of an otherwise replication-competent molecular clone of the FMuLV provirus. After transfection of this clone into cells that package the viral RNA in MuLV coats, infectious virus was released into the culture medium. Mouse fibroblasts infected with this virus, here called delta FMuLV, expressed the truncated viral env gene products in their cytoplasm but not on cell surfaces, and culture fluids from these cells did not transmit the infection to fresh mouse fibroblasts. In preliminary experiments, immunization of mice of H-2-congenic BALB/c strains with delta FMuLV conferred levels of immunity to FV disease ranging from weak to relatively strong. Immunized mice developed anti-FV IgM and IgG antibodies and cytotoxic T cells. Mice observed for 15 weeks after the first of two immunizations showed no detectable pathology, but delta FMuLV DNA was detectable in livers of some immunized mice for at least 3-6 weeks. These results suggest that our approach to development of retrovirus vaccines may be a useful one.

Animals↗