Search PubMed⌕ Search

Biomedical subjects

R V Gilden

Publications and source records attributed to R V Gilden.

At least 91 records · Page 5Linked to original sources
PubMed1976

Suppression of murine type-C RNA virogenes by type-specific oncornavirus vaccines: prospects for prevention of cancer.

Immunization of crossbred and F1 mice with combined killed and live Gross leukemia virus AKR type-C viral vaccines suppressed endogeneous N-type AKR virus up to 10,000-fold for significant periods during early life. Since several previous studies in the same and similar crossbred systems revealed direct correlations between low and high levels of type-C virus early in life with low and high incidences of leukemia and other cancers later in life, we believe that prospects for suppression of spontaneous neoplasms are good; however, 8-14 months will be required to achieve the final results. Should cancers be prevented by serotype-specific vaccines, such evidence would provide conclusive proof of endogenous viral etiology.

AKR murine leukemia virus↗
PubMed1976

Humoral immune responses of cats to feline leukemia virus: comparison of responses to the major structural protein p30 and to a virus-specific cell membrane antigen (FOCMA).

Radioimmunoprecipitation was used to test cat sera for ability to bind to the purified major internal protein p30 of feline leukemia viurs (FeLV), to the endogenous cat virus (RD-114), and to murine leukemia virus (MuLV). The data were compared with results of tests for antibody to the feline oncornavirus-associated cell membrane antigen FOCMA and for the presence of viremia. In contrast to the general lack of free antibody to FeLV p30 in a random sample of healthy cats, high levels of antibody to FeLV p30 and FOCMA were found in normal animals from high-leukemia-cluster households. Titers of greater than or equal to 200 for p30 and greater than or equal to 32 for FOCMA were found in nonviremic animals; a percentage of animals with high FOCMA titers and lower or no p30 binding activity were viremic. Animals with neoplasms were low or negative for FOCMA antibody and did not have high titers of free p30 antibody. The p30 binding activity could be divided into three main categories: high binding with FeLV p30 and much lower activity with RD-114 and MuLV p30's, as seen with hyperimmune sera; high binding with FeLV and RD-114 p30's and low activity with MuLV p30, possibly indicative of specific antibody to both of the aforementioned proteins; and low level binding to all three p30's.

Animals↗
PubMed1976

Inefficient humoral immune response of lymphoma-prone wild mice to persistent leukemia virus infection.

Adult wild mice (LC) from a natural colony with a high incidence of spontaneous lymphomas had free infectious virus in their seara (average 10(3.5) infectious units/ml) and parenchymal organs (average 10(5.2) infectious units/g tissue). They did not have detectable levels of free virus-specific antibodies that could be demonstrated by virus neutralization or immunofluorescence at higher than a 1:10 dilution. Only 5 of 28 animals had free antibodies detectable by radioimmunoprecipitation assay, and tissues of 4 mice also had nondetectable levels of virus determined by infectivity assay. Formalized vaccine from the indigenous virus did not induce production of virus-neutralizing antibodies or protect against naturally occurring disease. The animals with persistent leukemia virus infection, however, elicited good humoral immune responses to virus-unrelated antigen.

Animals↗
PubMed1976

Equine infectious anemia virus: evidence favoring classification as a retravirus.

Equine infectious anemia virus (EIAV) has a density of 1.154 g/cm3 in sucrose a high-molecular-weight RNA similar in size to Rauscher murine leukemia virus, and an internal virion reverse transcriptase that utilizes the synthetic RNA template poly(rA) but not the synthetic DNA template poly(dA), both with (dT)12 as primer. Although capable of utilizing manganese at low concentrations (approximately 0.1 mM), EIAV reverse transcriptase showed highest activity in the presence of 9 mM magnesium. The major protein of EIAV has a slightly lower molecular weight than the comparable protein of type C viruses and co-electrophoresed with 125I-labeled p25 of Mason-Pfizer monkey virus. A reference horse serum with antibodies to the major EIAV protein reacted only with EIAV and not with other type C or non-type C retraviruses. Reciprocally, a broadly reactive serum to type C virus p30s and specific sera to a variety of non-type C retraviruses did not react with EIAV. We recommend the inclusion of EIAV in the family Retraviridae.

Antigens, Viral↗
PubMed1975

Characterization of non-producer human cells induced by Kirsten sarcoma virus.

Non-producer (NP) human cells induced by the Kirsten sarcoma virus were characterized. These morphologically altered NP cells produced neither infectious virus nor complement-fixing antigens of the murine sarcoma-leukemia virus complex. The NP cells did not release RNA-dependent DNA polymerase and type-C virus particles with a density of approximately 1.15 g/ml in sucrose gradients by 3H-uridine labelling. The NP cells produced tumors when transplanted subcutaneously into athymic nude mice. The tumor cells re-established in culture resembled the orginal NP cells, were confirmed as human cells by karyological analysis and were also found to be "non-producer". The sarcoma virus genome in NP cells could be rescued not only by co-cultivation with "helper virus"-releasing cells but also by superinfection with helper type-C viruses. Murine (Rauscher, Ki-MuLV, AT-124 and two other xenotropic viruses), feline, RD-114 and Simian (woolly monkey and baboon) type-C viruses possessed the ability to rescue the sarcoma genome from NP cells but not AKR leukemia virus. In addition, the feline leukemia virus titer obtained by the rescuing technique in NP cells was the same as those obtained in feline embryo and NP cells by CF induction assay.

Animals↗
PubMed1975

Amino acid sequence homology of mammalian type C RNA virus major internal proteins.

The NH2-terminal amino acid sequence of the major group-specific antigen, the major internal virion protein (p30; approximate molecular weight 30,000) of several mammalian type C RNA viruses was determined by the Edman degradation procedure using an automated protein sequenator. All of the proteins analyzed show a high degree of over-all sequence homology and also contain specific regions or single residues. All p30s begin with the sequence prolyl-leucylarginyl (Pro-Leu-Arg) and have an invariant, conserved region from residues 11 to 24. In this region only a single amino acid difference appears between the cat and mouse p30s. At position 17 alanine is found in the cat, and serine in all the mouse proteins. This homologous region starts at position 10 for RD-114 and baboon virus p30s, and at position 18 in the protein of the virus isolated from gibbon ape. The region extending from residue 4 to 10 shows considerable variability between p30s isolated from different mammalian species. Out of 24 residues compared, only a single amino acid difference was found between six different mouse p30s. At position 4, three have leucine, two have alanine, and one has serine. The comparative sequence data demonstrate that the viral p30s are products of related genes in the viruses from various mammalian species.

Amino Acid Sequence↗
PubMed1975

Murine sarcoma virus related nucleic acid sequences in a non-transforming virus derived from an interspecies pseudotype sarcoma virus.

A number of sarcomagenic viruses recovered from hamster tumors induced originally by Moloney sarcoma virus or several of its mouse pseudotypes appear to be interspecies pseudotypes with structural proteins of hamster type-C viruses and nucleic acid sequences of both mouse and hamster specificity. A non-transforming virus (GLOH-minus) recovered from a sarcomagenic virus preparation obtained from a tumor induced by the Gross pseudotype of Moloney sarcoma virus was previously shown to retain mouse sequences. The ability to discriminate readily between Gross and Moloney viruses by molecular hybridization, especially with regard to thermal stability of inter-strain hybrid molecules, and the stability of Moloney virus sequences in a rat-mouse interspecies pseudotype, made it possible to specify that the mouse virus-specific sequences in GLOH-minus are derived from Moloney virus and not Gross. Thus, even though GLOH-minus is non-transforming in vitro or in vivo, it still retains sequences highly related to Moloney sarcoma virus. The lack of transforming ability is thus probably based on loss or change of specific sequences necessary for transformation at some point in the history of this virus.

AKR murine leukemia virus↗
PubMed1975

Transformation of horse skin cells by type-C sarcoma viruses.

A horse skin cell line (E. Derm, NBL-6, CCL-57) was susceptible to focus formation by the Kirsten mouse sarcoma virus, feline sarcoma virus (ST stain) and the MSV pseudotypes with woolly monkey, gibbon monkey, RD-114, AT-124, baboon placenta and murine xenotropic (BALB/c 3T3 and C57L/JD) type-C viruses. Foci were detected within 5 days after infection and the transformed cells continued to produce infectious virus and group-specific antigen of their respective type-C leukemia viruses. The transformation efficiency of various type-C sarcoma viruses in horse cells was also very high.

Animals↗
PubMed1975

Type-C virus-specific nucleic acid sequences in cultured rat cells.

Single-stranded DNA transcripts of rat type-C viruses prepared in the presence of actinomycin D, hybridized specifically to DNA of several rat cell cultures with no obvious qualitative or quantitative differences. Similar products prepared from a pseudo-type sarcoma virus with contributions from rat and mouse type-C viruses hybridized to both rat and mouse cellular DNA, while mouse viral transcripts did not hybridize to rat cell DNA. Viral RNA was detected in all rat cells by means of the rat viral DNA transcripts, with some differences between untreated low-passage cells and sister cultures treated with bromodeoxyuridine or bromodeoxyuridine and methylcholanthrene. Cells treated with both compounds were previously shown to be transformed and turorigenic, and these were distinguishable by kinetic analysis from the control cells.

Amino Acid Sequence↗
PubMed1975

Childhood sarcomas and lymphomas. Characterization of new cell lines and search for type-C virus.

Four cell lines were derived from childhood malignancies: rhabdomyosarcoma, sarcoma, lymphosarcoma and an American Burkitt's lymphoma. Cells of the four lines formed tumors in immunosuppressed newborn hamsters. The tumors had a microscopic appearance like that of the tumors from which the cell lines were derived. No virus-like particles were detected by electron microscopy in the cell lines after treatment with bromodeoxyuridine; no hamster type-C virus expression was present in cell lines derived from the hamster tumors. Chromosome constitution and in vitro growth properties of the cell lines were studied as was the fibrinolytic function of the sarcoma lines.

Adolescent↗
PubMed1975

Natural and experimentally induced antibodies to defined mammalian type-C virus proteins in primates.

Using sensitive radiommunoprecipitation assays for highly purified type-C RNA tumor virus proteins, we found that 5 of 16 clinically normal gibbons (including 4 of 5 normal animals from a colony with 2 cases of lymphoma) and 4 of 4 experimentally inoculated gibbons formed antibodies to the major structural protein (p30) of gibbon ape leukemia virus (GaLV). An additional woolly monkey immunized with the closely related simian sarcoma virus also formed antibodies detectable with GaLV p30. Of 20 patients immunized with formalin-inactivated Rauscher murine leukemia virus (R-MuLV), 10 were previously reported to have antibodies to MuLV as determined by an internally labeled banded virus radioimmunoprecipitation assay. In comparison studies with purified R-MuLV proteins, 7 of 20 patients formed antibodies: 3/20 to R-MuLV p30 only, 1/20 to R-MuLV glycoprotein (gp) 70 only, and 3/20 to both p30 and gp70. Most responders were melanoma patients receiving immunotherapy with BCG. Additionally, rhesus monkeys produced antibodies to the endogenous cat virus RD114 and closely related endogenous baboon leukemia virus p30's. Thus these studies demonstrated the ability of primates (including humans) to form antibodies to well-characterized proteins from endogenous and exogenous type-C viruses and the potential utility of these assays for seroepidemiologic studies.

Animals↗
PubMed1975

Characteristics of the major internal protein and RNA-dependent DNA polymerase of bovine leukaemia virus.

A virus designated bovine leukaemia virus (BLV), associated with leukaemia in cattle and previously demonstrated to induce the disease in sheep, was purified from chronically infected sheep cell cultures. Electrophoretic analysis showed a major protein of mol. wt. about 24,000 (p24) which reacted in gel diffusion and complement-fixation tests with sera from naturally infected cattle, experimentally infected sheep, and guinea pigs immunized with p24. BLV p24 has an isoelectric point of 8-6. Interspecies antigenic reactivities characteristic of mammalian Type C virus p30s were not detected in disrupted BLV or on p24. Sheep and guinea pig antisera to BLV, reactive with p24, also did not precipitate several Type C virus p30s in radioimmunoassays. BLV is also distinguished from Type C viruses and resembles mouse mammary tumour virus and Mason-Pfezer virus in having an RNA-dependent DNA polymerase which is preferentially active in the presence of Mg++ when synthetic templates are used. Along with previously published morphological data, the above indicates that BLV is not a Type C virus as classically defined. Four hundred and forty one human sera from cancer patients and matched controls were non-reactive with disruped BLV, BLV infected cells, and BLV p24 in complement-fixation tests.

Animals↗
PubMed1975

Effect of UV Light on RNA-Directed DNA Polymerase Activity of Murine Oncornaviruses.

The UV inactivation of RNA-directed DNA polymerase activity of Rauscher leukemia virus was shown to be due to damage to the protein. The UV dose resulting in 37% survival of viral polymerase activity at 254 nm was 2.4 x 10(4) to 3.1 x 10(4) ergs/mm(2). The inactivation rate of p30, a major internal viral protein, was much slower.

Journal Article↗