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PubMed1984

Generation of mink cell focus-forming viruses by Friend murine leukemia virus: recombination with specific endogenous proviral sequences.

A family of recombinant mink cell focus-forming viruses (MCF) was derived by inoculation of NFS mice with a Friend murine leukemia virus, and their genomes were analyzed by RNase T1-resistant oligonucleotide fingerprinting. The viruses were obtained from the thymuses and spleens of preleukemic and leukemic animals and were evaluated for dualtropism and oncogenicity. All these isolates induced cytopathic foci on mink cells but could be classified into two groups based on their relative infectivities for SC-1 (mouse) or mink (ATCC CCL64) cells. One group of Friend MCFs (F-MCFs) (group I) exhibited approximately equal infectivities for SC-1 and mink cells, whereas a second group (group II) infected mink cells 1,000- to 10,000-fold more efficiently than SC-1 cells. Structural analyses of the F-MCFs revealed that group I and group II viruses correlated with recombination of Friend murine leukemia virus with two distinct, but closely related, endogenous NFS proviral sequences. No correlation was found between the type of F-MCF and the tissue of origin or the disease state of the animal. Furthermore, none of the F-MCF isolates were found to be oncogenic in NFS/N or AKR/J mice. F-MCFs of both groups underwent extensive substitution of ecotropic sequences, involving much of the gag and env genes of group I F-MCFs and most of the gag, pol, and env genes of group II F-MCFs. All F-MCF isolates retained the 3' terminal U3 region of Friend murine leukemia virus. Comparison of the RNAs of the F-MCFs with RNAs of MCFs derived from NFS.Akv-1 or NFS.Akv-2 mice indicated that the F-MCFs were derived from NFS proviral sequences which are distinct from the sequences contained in NFS.Akv MCF isolates. This result suggested that recombination with particular endogenous proviral sequences to generate MCFs may be highly specific for a given murine leukemia virus.

Base Sequence↗
PubMed1987

Sequences responsible for erythroid and lymphoid leukemia in the long terminal repeats of Friend-mink cell focus-forming and Moloney murine leukemia viruses.

Despite the high degree of homology (91%) between the nucleotide sequences of the Friend-mink cell focus-forming (MCF) and the Moloney murine leukemia virus (MuLV) genomic long terminal repeats (LTRs), the pathogenicities determined by the LTR sequences of the two viruses are quite different. Friend-MCF MuLV is an erythroid leukemia virus, and Moloney MuLV is a lymphoid leukemia virus. To map the LTR sequences responsible for the different disease specificities, we constructed nine viruses with LTRs recombinant between the Friend-MCF and Moloney MuLVs. Analysis of the leukemia induced with the recombinant viruses showed that a 195-base-pair nucleotide sequence, including a 75-base-pair nucleotide Moloney enhancer, is responsible for the tissue-specific leukemogenicity of Moloney MuLV. However, not only the enhancer but also its downstream sequences appear to be necessary. The Moloney virus enhancer and its downstream sequence exerted a dominant effect over that of the Friend-MCF virus, but the enhancer sequence alone did not. The results that three of the nine recombinant viruses induced both erythroid and lymphoid leukemias supported the hypothesis that multiple viral genetic determinants control both the ability to cause leukemia and the type of leukemia induced.

Animals↗
PubMed1994

Contrasting effects from a single major histocompatibility complex class II molecule (H-2E) in recovery from Friend virus leukemia.

Resistance to erythroleukemia induced by infection with the Friend virus complex (FV) has been mapped to several genes residing both within and outside the murine major histocompatibility complex (MHC). MHC genes located in the A, D, and Qa/Tla regions of the murine H-2 complex have been shown to affect disease resistance through their capacity to regulate various aspects of the host immune response to viral antigens. This study establishes H-2E as the fourth MHC locus controlling immunological resistance to FV. Our investigation into the role of H-2E molecules revealed two distinct and opposite effects on recovery from Friend disease. H-2b/b mice normally lack a functional E gene product and are resistant to high doses of FV. The expression of H-2E molecules in H-2 recombinant or transgenic mice of this genotype resulted in a significant decrease in spontaneous recovery from FV-induced leukemia. In contrast, H-2E expression also appeared to influence recovery from Friend disease in a positive manner, since blocking these molecules with anti-E antibodies in vivo significantly decreased recovery from Friend disease. The data indicate that the positive effects of H-2E molecules derive from their function as restriction elements for helper T-cell recognition of the viral envelope glycoprotein, and we postulate that the negative effects are due to H-2E-dependent deletion in the T-cell repertoire during development.

Animals↗
PubMed2001

CD4(+) T cells and gamma interferon in the long-term control of persistent friend retrovirus infection.

We have used the Friend virus model to determine the basic mechanisms by which the immune system can control persistent retroviral infections. Previously we showed that CD4(+) T cells play an essential role in keeping persistent retrovirus in check. The present in vitro experiments with a Friend virus-specific CD4(+) T-cell clone revealed that these cells produce gamma interferon (IFN-gamma), which acts with two distinct mechanisms of antiviral activity. First, IFN-gamma had a direct inhibitory effect on virus production. This inhibitory effect was noncytolytic and, interestingly, was not associated with decreased cell surface expression of viral antigens. The second mechanism of IFN-gamma-mediated antiviral activity was an enhancement of CD4(+) T-cell-mediated cytolytic activity. We also found an in vivo role for IFN-gamma in the control of persistent Friend virus infections. Neutralization of IFN-gamma in persistently infected mice resulted in significantly increased levels of virus in the spleen, and a significant percentage of IFN-gamma-deficient mice were unable to maintain long-term control over Friend virus infections.

Animals↗
PubMed2001

Role of interleukin-4 (IL-4), IL-12, and gamma interferon in primary and vaccine-primed immune responses to Friend retrovirus infection.

The immunological resistance of a host to viral infections may be strongly influenced by cytokines such as interleukin-12 (IL-12) and gamma interferon (IFN-gamma), which promote T helper type 1 responses, and IL-4, which promotes T helper type 2 responses. We studied the role of these cytokines during primary and secondary immune responses against Friend retrovirus infections in mice. IL-4- and IL-12-deficient mice were comparable to wild-type B6 mice in the ability to control acute and persistent Friend virus infections. In contrast, more than one-third of the IFN-gamma-deficient mice were unable to maintain long-term control of Friend virus and developed gross splenomegaly with high virus loads. Immunization with a live attenuated vaccine virus prior to challenge protected all three types of cytokine-deficient mice from viremia and high levels of spleen virus despite the finding that the vaccinated IFN-gamma-deficient mice were unable to class switch from immunoglobulin M (IgM) to IgG virus-neutralizing antibodies. The results indicate that IFN-gamma plays an important role during primary immune responses against Friend virus but is dispensable during vaccine-primed secondary responses.

Animals↗
PubMed1993

Fusion of the erythropoietin receptor and the Friend spleen focus-forming virus gp55 glycoprotein transforms a factor-dependent hematopoietic cell line.

The Friend spleen focus-forming virus (SFFV) gp55 glycoprotein binds to the erythropoietin receptor (EPO-R), causing constitutive receptor signaling and the first stage of Friend erythroleukemia. We have used three independent strategies to further define this transforming molecular interaction. First, using a retroviral selection strategy, we have isolated the cDNAs encoding three fusion polypeptides containing regions of both EPO-R and gp55. These fusion proteins, like full-length gp55, transformed the Ba/F3 factor-dependent hematopoietic cell line and localized the transforming activity of gp55 to its transmembrane domain. Second, we have isolated a mutant of gp55 (F-gp55-M1) which binds, but fails to activate, EPO-R. We have compared the transforming activity of this gp55 mutant with the EPO-R-gp55 fusion proteins and with other variants of gp55, including wild-type polycythemia Friend gp55 and Rauscher gp55. All of the fusion polypeptides and mutant gp55 polypeptides were expressed at comparable levels, and all coimmunoprecipitated with wild-type EPO-R, but only the Friend gp55 and the EPO-R-gp55 fusion proteins constitutively activated wild-type EPO-R. Third, we have examined the specificity of the EPO-R-gp55 interaction by comparing the differential activation of murine and human EPO-R by gp55. Wild-type gp55 had a highly specific interaction with murine EPO-R; gp55 bound, but did not activate, human EPO-R.

Animals↗
PubMed2004

Relative contributions of perceived mattering to parents and friends in predicting adolescents' psychological well-being.

Perceived mattering is the psychological tendency to perceive the self as significant to specific other people. The central goal of this study was to examine whether adolescents' perceived mattering across social spheres (parents and friends) is addtive or compensatory in predicting adolescents' psychological well-being. Tests of the relative importance of adolescents' perceived mattering to parents and friends for psychological well-being were conducted using data from two convenience samples. Study 1 participants were, on the average, 17.5 yr. old and living in rural northwestern United States (N=128, 50% male, n=64; 50% female, n=64). Study 2 participants, on the average, were 16.9 yr. old, from a suburban western Canadian region (N=532, 51.4% male, n=273; 48.6% female, n=259). Hierarchical regression analysed with indicators of self-concept and behavioral misconduct as dependent variables used perceived mattering to parents and perceived mattering to friends and the interaction between these two variables as independent variables. Perceived mattering in both social spheres seemed the optimal condition for adolescents. Perceived mattering to friends "added" to perceived mattering to parents in explaining variance in assessments of psychological well-being in both studies.

Adolescent↗
PubMed1975

Treatment of runting syndrome and prevention of primary lymphomas in friend virus-tolerant rats.

A series of experiments showed that the inoculation of spleen and lymph node cells from rats immunized with Friend lymphoma (WFT-13) CELLS INTO Friend virus-tolerant rats induced the runting syndrome in nearly all cases, and immunological tolerance to WFT-13 was not broken in any survivors. However, th inoculation of specific immune spleen and lymph node cells admixed with normal bone marrow cells suppressed the runting death. In addition, in these animals the primary lymphomas that ordinarily occur about 200 days after neonatal inoculation of Friend virus did not appear. The mixture of immune spleen and lymph node cells and normal spleen and lymph node cells or normal thymus cells was ineffective in preventing the runting death or the incidence of primary lymphoma. Spleen and lymph node cells from normal rats or rats immunized with antigenically different AH-66 cells were also without effect. Spleen and lymph node cells from rats immunized with sheep red blood cells had a relatively high incidence of the runting syndrome; a few survivors rejected the WFT-13 transplants and also did not develop primary lymphomas. These results suggest that a supplement of hematopoietic stem cells from bone marrow eill not only prevent the runting death of Friend virus-tolerant rats produced by inoculating immune lymphoid cells but will also prevent the expected occurrence of primary lymphomas.

Animals↗
PubMed2002

Vocal behavior in the dyadic interactions of preadolescent and early adolescent friends and acquaintances.

Conversational interactions of sixth-grade friends and acquaintances in mixed- and same-gender pairs were computer analyzed so that the individual and dyadic time patterns of their vocal behavior could be examined. A comparison of their time patterns revealed that the boy-boy pairs used more and longer segments of simultaneous speech with acquaintances than with friends whereas the girl-girl pairs did the opposite. In general, partners tended to coordinate the durations of their vocal behaviors with each other but, more specifically, the boys coordinated the timing of their speaking turns and switching pauses more when they were friends than when they were acquaintances, and the girls again did the opposite. Finally, the girls coordinated the durations of their pauses significantly more than did the boys regardless of whether they were with friends or acquaintances or in mixed- or same-gender pairs.

Adolescent↗
PubMed1992

Nuclear protein kinase C activity is decreased in Friend erythroleukemia cells induced to differentiate.

Although it is well known that protein kinase C (PKC) is an important signaling molecule in Friend erythroleukemia cells it is not clear what role PKC may play in either regulated or unregulated erythroid cell proliferation and differentiation. The purpose of this study was to test the hypothesis that a decrease in nuclear PKC activity is associated with the induction of differentiation in Friend erythroleukemia cells. The effects of staurosporine, a selective inhibitor of PKC, and the tumor promoter, 12-O-tetradecanoyl phorbol-13-acetate, an activator of PKC, on Friend cell proliferation and differentiation were examined. Neither the inhibitor nor the activator of PKC affected proliferation at 96 h as measured by [3H]thymidine incorporation, but both compounds inhibited cell differentiation. In addition, nuclear PKC activity was highest in untreated and in tumor promoter-treated cells that were not differentiated, and it was lowest in cells induced to differentiate with hexamethylene bisacetamide or dimethylsulfoxide. It is concluded that nuclear PKC activity is essential for Friend erythroleukemia cell proliferation, and that a decrease in enzyme activity within the nucleus is associated with differentiation.

Acetamides↗
PubMed2005

Sources of exposure to smoking and drinking friends among adolescents: a behavioral-genetic evaluation.

Substance-using friends expose adolescents to models of, and opportunities for, substance use that may lead to its initiation or reinforce existing use. Using genetically informative data from the National Longitudinal Study of Adolescent Health (P. S. Bearman, J. Jones, & J. R. Udry, 1998), the authors examined whether adolescents' exposure to friends' tobacco smoking and alcohol drinking was better explained by family-social or genetic influences. To conduct analyses, the authors constructed substance use exposure scores for adolescent siblings from the responses of siblings' nominated friends to self-reported smoking and drinking items. Using behavioral-genetic analyses of these substance use exposure scores, the authors estimated that 64% of the variance in adolescents' exposure to friends who smoke and drink could be explained by genetic influences, whereas shared environmental influences were zero. These results provide evidence of active, evocative, or both types of gene-environment correlations. Genetic factors can influence the formation of friendships with substance-using peers, thereby contributing to adolescents' exposure to substance use behaviors.

Adolescent↗
PubMed1990

Regulation of the expression of the regulatory subunit of cAMP-dependent protein kinase II beta in Friend erythroleukemic cells. Evidence for posttranscriptional control and a central role for the C subunit.

Friend erythroleukemic cells provide a system for studying the regulation of the expression of regulatory (R) and catalytic (C) subunit isoforms of cAMP-dependent protein kinases. Friend cells contain RI alpha, two RII subunits previously designated RII-52 and RII-54, and C alpha. When the cells are treated with 0.2 mM methylisobutylxanthine (MIX) and either 20 microM forskolin or 0.5 mM 8-Br-cAMP, RI alpha content declines 50-75% because of a large decrease in the t1/2 value for the dissociated RI alpha subunit; RII-54 expression is invariant, but the amount and rate of synthesis of RII-52 increases 10-15-fold (Schwartz, D. A., and Rubin, C. S. (1985) J. Biol. Chem. 260, 6296-6303). We now demonstrate that RII-52 and RII-54 correspond to RII beta and RII alpha, respectively. When cAMP levels are elevated in Friend cells the abundance of the 3.3-kilobase RII beta mRNA increases 25-30-fold in parallel with the rate of RII beta subunit synthesis indicating that pretranslational control is operative. Other R and C mRNAs are not markedly induced. Surprisingly, the rate of transcriptional initiation of the RII beta gene and the stability of RII beta mRNA are not altered during RII beta induction. Rather, the induction of RII beta mRNA is associated with the accumulation of major (3.4 kilobases) and minor (4 kilobases) RII beta pre-mRNAs in the nucleus. It appears that the cAMP signal-transduction system alters a nuclear protein(s) such that either the proportion of RII beta pre-mRNAs that are processed to mature mRNAs and are exported to the cytoplasm is greatly increased or the nuclear precursors are stabilized. Thus, regulation is exerted at a posttranscriptional level. In order to establish directly a causal role for C in RII beta induction and to rule out artifacts introduced by the use of drugs such as forskolin, MIX, and cAMP analogs we stably transfected Friend cells with a vector containing C alpha cDNA under the regulation of the zinc-activated metallothionein I promoter. The addition of 0.15 mM ZnSO4 caused the accumulation of dissociated C subunits and the selective induction of RII beta.

1-Methyl-3-isobutylxanthine↗
PubMed1991

Erythropoietin activates the receptor in both Rauscher and Friend murine erythroleukemia cells.

Alterations in the expression of two proto-oncogenes, c-myb and c-myc, have been implicated in the differentiation of transformed erythroid cells induced by chemical inducers, such as dimethyl sulfoxide (Me2SO). In the present study, we compared the expression of c-myb and c-myc during erythropoietin (Epo) and Me2SO induction of Rauscher erythroleukemia cells, which differentiate in response to both inducers, and Friend erythroleukemia cells, in which Epo-induced differentiation is blocked. Our results demonstrate that Epo induces specific changes in expression of c-myb and c-myc in both Rauscher and Friend cells. Epo increases c-myc transcript, in contrast to a decreased caused Me2SO, indicating that the biphasic mode of c-myc regulation seen with Me2SO is not required for erythropoiesis. The Epo-induced changes in c-myb and c-myc do not require new protein synthesis, thus identifying these proto-oncogenes as early response genes for Epo. Both cell types also exhibit rapid changes in membrane protein phosphorylation in response to Epo. Since the signal pathway from Epo receptor activation to the nucleus appears equally functional in both Rauscher and Friend cells, the data suggest that the inability of Friend cells to differentiate in response to Epo is due to a block at a later step in the induction process.

Animals↗
PubMed1990

Spi-1 oncogene activation in Rauscher and Friend murine virus-induced acute erythroleukemias.

The Friend viruses, like the Rauscher virus, cause murine acute erythroleukemias which evolve in a similar multistep process. In previous studies it has been described that the late malignant proerythroblastic transformation induced by the polycythemia-inducing strain of Friend spleen focus-forming virus (SFFVP) is correlated with Spi-1 oncogene activation by insertional mutagenesis. In this paper we report that Spi-1 genomic rearrangements were also observed in 90% of tumors induced by the anemia-inducing strain of Friend spleen focus-forming virus (SFFVA) and in all Rauscher-induced tumors analyzed. SFFVA and Rauscher proviral insertions occurred in the viral integration cluster previously characterized in SFFVP-induced tumors. The Spi-1 1.4-Kb messenger RNA was found highly expressed in all SFFVA and Rauscher-induced malignant cells as compared to normal tissues. The nucleotide sequence of Spi-1 cDNA isolated from a library constructed from SFFVA-induced tumor cells revealed no difference between the Spi-1 gene transcripts expressed in both SFFVP and SFFVA-induced leukemic cells. These results indicate that Spi-1 gene activation is a general feature in the malignant proerythroblastic transformation which occurs in mice infected with Friend and Rauscher viruses.

Acute Disease↗
PubMed1988

Inactivation of the p53 oncogene by internal deletion or retroviral integration in erythroleukemic cell lines induced by Friend leukemia virus.

The p53 gene is rearranged in a high proportion of erythroleukemic cell lines derived from the spleens of mice infected with Friend leukemia virus. These rearrangements result in either the synthesis of a truncated protein or the inactivation of the p53 gene. Here we have molecularly characterized the rearrangements in two murine erythroleukemic cell lines induced by Friend leukemia virus, DP20-1 and CB3, that contain a rearranged p53 gene and fail to express p53 protein. The rearrangement in the DP20-1 cell line is due to the insertion of Friend spleen focus-forming provirus (SFFV) in the 3' end of the p53 gene in intron sequences between exons 9 and 10. Transfection of molecular clones of this SFFV provirus into NIH3T3 cells results in the generation of infectious virus as determined by its ability, in the presence of helper virus, to induce rapid splenomegaly and polycythemia when injected into adult DBA/2J mice. Insertion of SFFV in DP20-1 cells resulted in the expression of an aberrant 2.9 kb RNA species. Analysis of a molecular clone of the rearranged p53 gene in a second cell line, CB3, revealed that the p53 gene in this clone has sustained a large deletion within the p53 gene resulting in the loss of coding sequences between exons 4 and 8. The 5' end of the deletion originates within exon 4 and extends 3' to within the eighth intron. The significance of these findings with regard to the multi-stage nature of Friend virus induced erythroleukemia is discussed.

Animals↗
PubMed1977

Interactions of rodent malarial parasites with Friend erythroleukemia cells in vitro.

The ability of Plasmodium chabaudi and P. yoelii to bind to Friend erythroleukemia cells in vitro was examined. Extensive binding of P. yoelii and weaker binding of P. chabaudi was observed. Binding to mouse fibroblasts was not seen, although there was some binding to cells of a mouse mastocytoma. The binding of P. yoelii to Friend cells was sensitive to specific antiserum. The development of P. berghei and P. yoelii in Friend cells was followed by microscopic examination and measurement of the infectivity of those cells in mice. Friend cells infected with both species appeared to develop morphologically normal intracellular forms of the parasites. P. yoelii-infected cells were infective in sensitive mice for 3 days after addition of the parasites, and this infectivity was not sensitive to treatment in vitro with mouse anti-P. yoelii serum.

Animals↗
PubMed1979

Erythroid leukemia induced by Friend lymphatic leukemia virus in T-cell-depleted mice.

BALB/c mice depleted of T-cells by thymectomy at 3 to 5 days of age and by treatment with antithymocyte serum were inoculated with the lymphatic leukemia virus derived from Friend virus. After a long latent period, these animals developed erythroid leukemia. In contrast, intact control mice inoculated with Friend virus-associated lymphatic leukemia virus developed typical thymic (T-cell) lymphomas. Cell-free virus prepared from leukemic T-cell-depleted animals induced lymphoid, myeloid, and erythroid leukemias in intact mice. The erythroid leukemia-inducing virus differed from the spleen focus-forming component of Friend virus in its long latent period (88 to 225 days) and in its inability to induce spleen foci. End-point dilution experiments suggested that a hitherto undescribed component of the Friend virus complex might be responsible for these late-appearing erythroid leukemias.

Animals↗
PubMed1981

Beta 2 receptor-mediated stimulation of Friend erythroleukemia cell growth by thyroid hormones.

Thyroid hormones are known to enhance normal erythroid colony growth (CFUE) and this enhancement depends on a functional beta 2-adrenergic receptor mechanism. we investigated the response of Friend cells to thyroid hormones, catecholamines, and other compounds influencing cellular cAMP activity. The thyroid hormones L-T3, L-T4, and "reverse T3" stimulated erythroleukemia colony growth in a serum-substituted methylcellulose culture system with peak activity at 10(-7) M. Various beta-adrenergic compounds enhanced Friend leukemia colony growth; however, the alpha-adrenergic agonist phenylephrine was inactive. Dibutyryl cyclic AMP and the phosphodiesterase inhibitor theophylline also enhanced Friend leukemia colony formation. Adrenergic antagonists with beta 2 specificity abrogated the stimulatory effect of L-T3, L-T4, and of "reverse T3" at equimolar concentrations. These experiments demonstrate that thyroid hormones, beta-adrenergic agonists, the phosphodiesterase inhibitor theophylline, and dbcAMP have a direct effect on the proliferation of Friend erythroleukemia cells. We conclude that thyroid hormones' action requires a functioning beta 2-adrenergic receptor mechanism. Thyroid hormones directly modulate the growth of neoplastic erythroid cells in a manner consistent with their effects on normal erythropoiesis.

Animals↗