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Biomedical subjects

B Chesebro

Publications and source records attributed to B Chesebro.

At least 127 records · Page 7Linked to original sources
PubMed1985

Different murine cell lines manifest unique patterns of interference to superinfection by murine leukemia viruses.

Interference to superinfection by murine leukemia viruses (MuLV) was analyzed in cells chronically infected with other MuLVs. A new sensitive focal immunofluorescence assay employing monoclonal antibodies was used to detect foci of virus infection in live cell monolayers. Monoclonal antibodies were chosen which reacted with the challenge virus but not with the interfering virus. The results obtained confirmed some of the findings of previous workers using Moloney sarcoma virus pseudotypes as challenge viruses on mouse and nonmouse cells. In addition, SC-1 mouse cells nonproductively infected with defective spleen focus-forming virus were found to be resistant to superinfection by recombinant dual-tropic viruses. Furthermore, results indicated that interference patterns between some pairs of viruses differed in different cell types. Thus, xenotropic MuLV blocked superinfection by recombinant dual-tropic viruses in SC-1 feral mouse cells, but not in two lines of NZB mouse cells. Also, in a Mus dunii tail fibroblast cell line some unique patterns of interference were observed. One ecotropic MuLV blocked infection by two xenotropic viruses and three recombinant dual-tropic viruses. Two other ecotropic viruses blocked infection by only one of the two xenotropic viruses tested. These two ecotropic viruses also differed from each other in their ability to block the three recombinant viruses. In addition, two strains of amphotropic MuLV also differed in their interference capacity. As expected, strain 1504A did not block any viruses tested, whereas strain 4070A surprisingly blocked one xenotropic and one ecotropic MuLV. The lack of homogeneity in interference patterns seen in the Mus dunii cells suggested either that a large number of heterogeneous virus receptors were present on this cell line or that interference in these cells might operate through a mechanism other than blocking of virus receptors by the envelope protein of the interfering virus.

Animals↗
PubMed1984

Identification of a unique erythroleukemia-associated retroviral gp70 expressed during early stages of normal erythroid differentiation.

Late in the course of Friend virus (FV)-induced erythroleukemia, leukemic spleen cells express a cell surface retroviral gp70 envelope protein not detected during the early proliferative phase of the disease. Characterization of this gp70 revealed it was unrelated to the input Friend murine leukemia virus (F-MuLV), but antigenically similar to a unique subset of endogenous xenotropic viruses. This gp70 was expressed by murine erythroleukemia cell lines but has not been identified on cell lines of other lineages. A monoclonal antibody (18-6) specifically reactive with this polypeptide was used to examine hematopoietic organs of normal uninoculated mice. This antibody detected a gp70 expressed by a majority of erythroid cells in fetal liver and by a small but significant percentage of normal adult spleen and bone marrow cells. Increased erythropoietic activity induced by treatment of adult mice with phenylhydrazine ( PHZ ) resulted in a seven- to eightfold increase in the frequency of spleen and bone marrow cells expressing this gp70. Peptide map analysis indicated that the 18-6 reactive gp70 expressed by Friend erythroleukemia cells and by cells from normal fetal liver were structurally identical. These results suggested that this unique gp70 was an erythroid-specific differentiation antigen.

Animals↗
PubMed1984

Murine resistance to street rabies virus: genetic analysis by testing second-backcross progeny and verification of allelic resistance genes in SJL/J and CBA/J mice.

Intraperitoneal challenge with street rabies virus of second-backcross offspring produced from susceptible females mated with either randomly selected or rabies-resistant first-backcross males indicated that murine resistance is under the influence of the concurrent presence of each of two segregating genes. Furthermore, the greater than or equal to 96% resistance of offspring produced from (SJL X CBA)F1 and (CBA X SJL)F1 hybrids crossed to susceptible A.SW or A/WySn mice demonstrated that resistance genes of SJL/J and CBA/J mice are allelic.

Alleles↗
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↗
PubMed1983

Effect of murine host genotype on MCF virus expression, latency, and leukemia cell type of leukemias induced by Friend murine leukemia helper virus.

Leukemias induced by neonatal inoculations of several mouse strains with different strains of Friend murine leukemia helper virus (F-MuLV) were followed for time of disease onset, cytochemical analysis of predominant cell types in leukemic organs, and expression of infectious mink cell focus-inducing (MCF) viruses detected by mink cell foci or MCF-specific monoclonal antibodies. Most BALB.B and IRW mice had a rapidly appearing, severe anemia and hepatosplenomegaly consisting of erythroid cells. MCF viruses were usually isolated from enlarged spleens of IRW mice. In contrast, C57BL/10 mice had a lower incidence of disease and much slower course. Splenomegaly and lymphadenopathy with mild anemia were seen, and the predominant cell types were either myeloid (chloroleukemia) or lymphoid. MCF viruses were never isolated from this mouse strain. (C57BL/10 X IRW)F1 mice were intermediate in latency, but all mice had disease by 8 months. Myeloid, lymphoid, and some mixed leukemias with an erythroid component were observed, but in no case did we see the severe anemia or pure erythroid involvement typical of IRW and BALB.B mice. MCF viruses were, however, isolated from 22% of these mice regardless of leukemia cell type. DBA/2 mice had a disease pattern similar to the (C57BL/10 X IRW)F1 mice, and MCF viruses were isolated from three of six mice tested. Inoculation of IRW mice with the low virulence B3 strain of F-MuLV produced disease with a longer latency than F-MuLV 57, but similar cell types were transformed by both viruses. In vitro cell lines were derived from 14 mice, and most were tumorigenic in vivo. Three lines released infectious MCF virus, and three others expressed MCF-specific cell surface antigens but did not release virus. Eight lines expressed no MCF infectious virus or viral antigens. Several lines released infectious xenotropic viruses and/or expressed xenotropic MuLV cell surface antigens recognized by monoclonal antibodies reactive with xenotropic viruses. The lack of MCF expression in many primary leukemic tissues as well as in in vitro derived leukemia cell lines of C57BL/10 and (B10 X IRW)F1 mice suggested that MCF virus generation and expression may not be required for leukemogenesis in some mouse strains or in some hemopoietic lineages.

Animals↗
PubMed1983

H-2D control of recovery from Friend virus leukemia: H-2D region influences the kinetics of the T lymphocyte response to Friend virus.

A Friend virus (FV)-specific T lymphocyte proliferation assay was used to compare the T lymphocyte responses of H-2 congenic mice that differed in their ability to recover from FV leukemia after inoculation of high virus doses. Gene(s) of the H-2D region influenced the kinetics of this response such that H-2Db/b homozygous mice were positive 6-8 d earlier than H-2Dd/b mice. This correlated with the Rfv-1, H-2D-linked influence on recovery from FV by these mice, and also appeared to explain the prominent effect of virus dose on recovery incidence. These findings were supported by the ability of passively transferred immune splenic T lymphocytes to induce recovery from leukemia at 6 d after FV inoculation, but not at 16 d. H-2a/a mice were found to be unresponsive in the FV-specific T lymphocyte proliferation assay. This effect mapped to the left of H-2D, possibly in the H-2I region, and may be an in vitro manifestation of the Rfv-2 gene. No evidence for nonspecific immunosuppression of the T lymphocyte response to concanavalin A was observed in any of the H-2 congenic F1 mice studied.

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↗
PubMed1983

Use of monoclonal anti-gp70 antibodies to mimic the effects of the Rfv-3 gene in mice with Friend virus-induced leukemia.

During the course of progressive Friend virus-induced leukemia in Rfv-3r/s mice, antiviral antibody caused a marked reduction in the frequency of leukemic spleen cells releasing infectious virus. We investigated the mechanism of this antibody-induced alteration of leukemia cell phenotype in a series of passive transfer experiments using monoclonal antiviral antibodies. Our results indicated that two IgG2a anti-gp70 cytotoxic antibodies could reduce the frequency of virus-producing cells within the leukemic spleen as well as maintain the virus-nonproducing phenotype once it was established. IgG2a and IgG2b monoclonal anti-p 15 antibodies, IgM, and IgA anti-gp70 antibodies, and an IgG3 anti-p 15(E) antibody were not effective. The mechanism of this phenotypic alteration appeared to involve an antibody-mediated cytostasis of virus-producing leukemia cells with the subsequent over-growth of virus-nonproducing cells. The maintenance of the virus-nonproducing phenotype was dependent on the presence of anti-gp70 antibodies capable of neutralizing and clearing infectious F-MuLV in vivo. The presence of these neutralizing antibodies appeared to prevent reinfection of virus-nonproducing cells and therefore interfered with reversion to the virus-producing phenotype.

Animals↗
PubMed1982

MCF-specific murine monoclonal antibodies made against AKR-247 MCF virus recognize a unique determinant associated with the gp70-p-15(E) complex.

Hybridomas obtained from (NFS X AKR)F mice immunized with syngeneic cells infected with AKR-247 MCF virus produced antibodies specific for only AKR-247 or closely related MCF viruses which hare a previously defined MCF antigen (MCFA-3). These monoclonal antibodies recognized a new type of viral antigenic determinant which appeared to be a conformational determinant associated with the env precursor polyprotein (pr80env) or its disulfide-linked gp70-p15(E) complex (gp80) but not with free gp70 or p15(E) or any other virion or virus-induced protein.

AKR murine leukemia virus↗
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↗
PubMed1981

Replication-defective Friend murine leukemia virus particles containing uncleaved gag polyproteins and decreased levels of envelope glycoprotein.

An erythroleukemia cell clone, 7C, which failed to produce reverse transcriptase-containing virions or infectious virus, was found to produce noninfectious virus particles by gradient banding of [3H]leucine- and [3H]uridine-labeled virions. The RNA from the 7C virus was shown to consist of the normal 70S size component, which converted to 35S upon heat denaturation. In contrast, the 7C virion proteins showed multiple defects. Analysis of the virion proteins by gel electrophoresis demonstrated that the pr65 gag precursor was incorporated into the 7C virus and that the processing of this precursor was severely diminished. Polymerase proteins pr180gag-pol and pr120pol were also detected in virions, and a third possible polymerase protein, p70, was reduced in size compared to its normal counterpart, p80. Incorporation of the viral gp70 glycoprotein into particles was also reduced 10-fold, despite synthesis and incorporation of gp70 into the 7C cell membrane in normal amounts. Pulse-chase analysis of the synthesis of the viral gag and env proteins in 7C cells showed greatly reduced amounts of pr180gag-pol, pr65gag, p80gag, and p42gag, whereas pr90env, gp70, and spleen focus-forming virus-specific gp55 were synthesized and processed normally. These results suggested that at least one defect in 7C virus was impaired cleavage of gag or pol proteins or both, most likely due to a lack of the appropriate viral protease, and that this lack of cleavage might affect incorporation of gp70 into virus particles.

Animals↗
PubMed1980

H-2D (Rfv-1) gene influence on recovery from Friend virus leukemia is mediated by nonleukemic cells of the spleen and bone marrow.

H-2D (Rfv-1)-associated control of recovery from FV leukemia was studied in congenic mice. In irradiation chimeras, the high recovery phenotype was transferred by cells of the spleen, bone marrow, and fetal liver. Furthermore, in cell transfers using unirradiated recipients, spleen and bone marrow cells of the high-recovery genotype were able to mediate recovery from leukemia in mice of the low-recovery genotype. Thus, the H-2D (Rfv-1) influence on recovery appeared to operate via nonleukemic cells of the spleen and bone marrow rather than via leukemic cells. The specific nonleukemic cell type(s) involved in recovery remains unknown. However, the mechanism appears to be complex and probably involves both anti-FV antibody and FV-specific cytotoxic T lymphocytes.

Animals↗
PubMed1980

Spontaneous cessation of Friend murine leukemia virus production by leukemia cell line Y57: overgrowth by nonproducer cells.

Cell line Y57, obtained from a (C57BL/10 X A.BY)F1 mouse made leukemic with Friend virus complex (FV), spontaneously ceased FV production in vitro after 20 passages. By limiting dilution cloning, the incidence of non-virus-producing cells was found to increase with sequential passage. Nonproducer cells apparently arose spontaneously and were able to increase in number relative to producer cells because the growth rate of nonproducer cells was more rapid than the rate at which virus could reinfect them. Nonproducer clones all contained the defective spleen focus-forming virus in a latent but rescuable form but showed defects in helper virus env and gag gene product synthesis. Stable long-term virus-producing clones were obtained both by cloning at early in vitro passages or by cloning immediately after reinfection of nonproducer cells with FV.

Animals↗
PubMed1979

Anti-Friend virus antibody is associated with recovery from viremia and loss of viral leukemia cell-surface antigens in leukemic mice. Identification of Rfv-3 as a gene locus influencing antibody production.

A single genetic locus, Rfv-3, influenced Friend virus (FV) viremia, loss of FV-induced cell-surface antigens from leukemia cells, and generation of anti-FV antibodies. 30--90 d after FV infection leukemic spleen cells from (B10.A X A)F1 and (B10.A X A.BY)F1 mice (Rfv-3r/s) were found to have low FV-induced cell-surface antigen expression compared to leukemic spleen cells from A and A.BY mice (Rfv-3s/s). In addition, these F1 mice recovered from viremia and generated cytotoxic anti-FV antibodies. A and A.BY mice did not recover from viremia and failed to generate anti-FV antibodies. Anti-FV leukemia cell antibody appeared to mediate FV-antigen loss because decrease of FV cell-surface antigens occurred at the same time as anti-FV antibody appeared in the plasma of F1 mice, and passive transfer of anti-FV antisera induced modulation of FV cell-surface antigens. Rfv-3 did not influence an intrinsic ability of FV antigens to be modulated from Rfv-3s/s leukemia cells because FV antigen loss from Rfv-3s/s spleen cells occurred after transfer of cells to an immune environment.

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