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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↗
PubMedDate not supplied

Old friends, new friends: predictors of children's perspective on their friends at school.

Predictors of 5-year-old kindergartners' insights into their friends, and their accounts of liking and conflict with their friends were investigated, with a focus on both the children's and their friends' social understanding during the preschool period, and the quality of their preschool friendships. Seventy children initially studied at 4 years utilizing social cognition tasks and observations of dyadic play with their friends were followed over the transition to school; at school they were interviewed about their friendships and their social understanding was assessed. One group had remained close to their preschool friends, whereas a second group had formed new friendships. Social understanding, language abilities, and prosocial characteristics of both the children and preschool friends, their successful communication and shared pretend play experiences during the preschool period, and their mothers' educational level were related to their perspectives on their current school friends. Liking of current friends was linked to relationship history and maternal educational level for both those with old and with new friends, whereas insight was related to assessments of social cognition.

Awareness↗
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↗
PubMed2004

Friends don't let friends ...or do they? Developmental and gender differences in intervening in friends' ATOD use.

This study focused on the strategies adolescents endorsed for situations in which friends were experimenting with alcohol, tobacco, and other drugs. Four hypothetical vignettes (concerning a friend smoking, using drugs, getting drunk at a party, or deciding whether to attend a party with alcohol and drugs) were presented to 2697 5th-12th graders. Whereas younger students were more likely to choose proactive strategies (talking to the friend or an adult or ending the friendship), older students were more inclined to say they would ignore a friend's smoking and drug use although they would take the car keys away from a friend drinking alcohol. Among those 13 years old and older, the more dangerous the substance, the more inclined the youth were to intervene. Females were more inclined than males to talk to friends about smoking, drinking, and drugs and less inclined to ignore the behaviors or stop being a friend.

Adolescent↗
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↗
PubMedDate not supplied

Assessing friend support of adolescents' diabetes care: the diabetes social support questionnaire-friends version.

OBJECTIVE: To develop and evaluate the Diabetes Social Support Questionnaire for Friends (DSSQ-Friends), a measure of friends' supportive behaviors for adolescents with diabetes. Gender and age differences in friends' support for diabetes were examined, as well as the relationship between friend support and adolescents' treatment adherence. METHODS: Seventy-four adolescents (11-18 years) completed the DSSQ-Friends in addition to other measures of social support and a measure of treatment adherence. The behaviors on the DSSQ-Friends were scored for supportiveness and frequency. A combined rating (frequency x support) was also calculated to adjust the frequency of friends' support for adolescents' perceptions of supportiveness. RESULTS: The DSSQ-Friends had acceptable internal consistency and good test-retest reliability; it correlated well with other measures of friend support. Age-related differences were minimal; however, compared to boys, girls reported more friend support for blood glucose testing and emotions. Friend support was not related to overall treatment adherence but was related to adherence for blood glucose testing. CONCLUSIONS: We discuss the utility of the DSSQ-Friends as a clinical and research tool for measuring diabetes-specific friend support and offer suggestions for future research on friends' support for adolescents' diabetes care.

Adolescent↗
PubMed2006

Attributions of adolescents with type 1 diabetes related to performing diabetes care around friends and peers: the moderating role of friend support.

OBJECTIVE: To examine the relationships among negative attributions of friend and peer reactions to diabetes management in social situations, anticipated adherence difficulties, friend support, diabetes stress, and metabolic control. METHODS: A sample of 102 adolescents with Type 1 diabetes completed instruments measuring attribution of friend and peer reactions, anticipated adherence, friend support, and diabetes stress. Metabolic control was measured by the percentage of hemoglobin A1c. RESULTS: Structural equation modeling demonstrated an excellent fit of two models depicting the mediating role of anticipated adherence difficulties and diabetes stress on the relationship between negative attributions of friend (first model) and peer (second model) reactions and metabolic control. Friend support was found to moderate the path between diabetes stress and metabolic control in an unexpected manner. That is, as friend support increased, so did the relationship between stress and metabolic control. CONCLUSIONS: Adolescents who make negative attributions about reactions of friends and/or non friend peers are likely to find adherence difficult in social situations and have increased stress, with the latter associated with metabolic control. Results are discussed in terms of a social information processing model of adjustment.

Adolescent↗
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↗
PubMed2005

Activation of the Jun N-terminal kinase pathway by friend spleen focus-forming virus and its role in the growth and survival of friend virus-induced erythroleukemia cells.

Members of the mitogen-activated protein kinase (MAPK) family, including Jun amino-terminal kinase (JNK) and extracellular signal-related kinase (ERK), play an important role in the proliferation of erythroid cells in response to erythropoietin (Epo). Erythroid cells infected with the Friend spleen focus-forming virus (SFFV) proliferate in the absence of Epo and show constitutive activation of Epo signal transduction pathways. We previously demonstrated that the ERK pathway was constitutively activated in Friend SFFV-infected erythroid cells, and in this study JNK is also shown to be constitutively activated. Pharmacological inhibitors of both the ERK and JNK pathways stopped the proliferation of primary erythroleukemic cells from Friend SFFV-infected mice, with little induction of apoptosis, and furthermore blocked their ability to form Epo-independent colonies. However, only the JNK inhibitor blocked the proliferation of erythroleukemia cell lines derived from these mice. The JNK inhibitor caused significant apoptosis in these cell lines as well as an increase in the fraction of cells in G(2)/M and undergoing endoreduplication. In contrast, the growth of erythroleukemia cell lines derived from Friend murine leukemia virus (MuLV)-infected mice was inhibited by both the MEK and JNK inhibitors. JNK is important for AP1 activity, and we found that JNK inhibitor treatment reduced AP1 DNA-binding activity in primary erythroleukemic splenocytes from Friend SFFV-infected mice and in erythroleukemia cell lines from Friend MuLV-infected mice but did not alter AP1 DNA binding in erythroleukemia cell lines from Friend SFFV-infected mice. These data suggest that JNK plays an important role in cell proliferation and/or the survival of erythroleukemia cells.

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↗