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R C Mellors

Publications and source records attributed to R C Mellors.

At least 19 recordsLinked to original sources

Leukemia serum reactive with retrovirus-related antigen in normal human placenta.

Serum antibody reactive with a retrovirus-related p30 antigen in human normal term placenta was investigated and characterized by immunohistologic and immunoblotting methods. Sera obtained from patients with acute leukemia and malignant lymphoma were used as first antibody, and cryostat sections of placenta were the target antigen. An IgM antibody that reacted mainly with the basal aspect of syncytiotrophoblast of chorionic villi, where a putative human endogenous retrovirus p30 antigen is located, was directed by indirect immunofluorescence. This antibody activity, termed anti-basal aspect of syncytiotrophoblast (anti-BAST), was detected in the sera of many patients with acute leukemia (AML, ALL) and malignant lymphoma, and less frequently in sera of pregnant women and normal controls. As shown by immunoblotting analysis, the main reactive antigen recognized by anti-BAST was a non-glycosylated 32-kDa placental protein which was antigenically related to SSAV p30. A non-glycosylated 19-kDa protein was also considered to be one of the anti-BAST-corresponding antigens. This suggests the presence of a new antigen-antibody system of human retrovirus(es) revealed by subinfectious antigenic expression and by specific antibody activity in conditions of human health and disease, particularly, acute leukemias and malignant lymphomas of common types.

Antibody Specificity

Detection and immunochemical characterization of a primate type C retrovirus-related p30 protein in normal human placentas.

We find that 12 of 14 specimens of normal human term placentas analyzed by one- or two-dimensional electrophoresis and immunoblotting contain a protein or polypeptide of approximately equal to 30,000 daltons that is antigenically cross-reactive with p30 core protein of the simian sarcoma-associated virus/gibbon ape leukemia virus primate retrovirus group and is physicochemically similar to reference murine and primate type C retrovirus p30s. This finding may lead to an understanding of endogenous type C retrovirus gene expression in humans.

Antibodies, Viral

Immunohistologic detection of antigen related to primate type C retrovirus p30 in normal human placentas.

This study reports the immunohistologic detection of SSAV/GaLV type C retrovirus p30-related antigen in unfixed cryostat sections of normal human term placentas by the indirect immunofluorescence method. Goat anti-SSAV p28 serum reacted specifically with 10 of 10 anatomic specimens of human placenta. Goat anti-GaLV p29 serum reacted similarly with 8 of 10 specimens. Goat anti-BaEV p28, anti-RD-114 p28, anti-FeLV p27, anti-R-MuLV p30, and anti-MPMV p27 gave no specific reaction with placenta. The anti-SSAV p28 and anti-GaLV p29 reactive antigen was located in the placenta mainly at the basal aspect of syncytiotrophoblast near the underlying trophoblastic basement membrane where type C retroviruslike particles have been found electronmicroscopically. The specific antibody activity of anti-SSAV p28 serum against placenta was removed by critical absorption with disrupted SSAV or GaLV but not RD-114 or MuLV. These results suggest the presence in human placenta of a putative type C retroviral protein which cross-reacts with the p30 protein of the SSAV/GaLV type C retrovirus group.

Animals

Structural heterogeneity in p30 molecules of type C viruses.

Tryptic digests of p30 proteins from mouse type C viruses were subjected to cation-exchange chromatography. Structural heterogeneity of p30 molecules was seen in two specific areas of the peptide elution profiles. These hypervariable regions of p30 proteins were used to discriminate representative ecotropic (N- and B-tropic), xenotropic (alpha and beta) and amphotropic viruses.

Animals

Tryptic peptide analysis of gag gene proteins of endogenous mouse type C viruses.

Tryptic digests of the internal proteins p30, p15, p12, and p10 of mouse xenotropic, ecotropic, and amphotropic type C viruses were subjected to cation-exchange chromatography. Analysis of these maps revealed that the p30 proteins from representative isolates of all three viral subgroups were distinguishable. The p15 proteins were all unique. The p12 proteins of NZB xenotropic and wild-mouse amphotropic viruses were not identical and yielded peptide maps remarkably different from that of the ecotropic virus. The p10 proteins of xenotropic and ecotropic viruses were identical and were dissimilar to that of the wild-mouse amphotropic virus.

Animals

Type C RNA virus expression in systemic lupus erythematosus. New Zealand mouse model and human disease.

An antigen recognized by antisera produced against p30 (core) proteins of the four chief groups of mammalian type C viruses (murine, feline, RD-114 related to endogenous primate, and infectious primate group) is located in an immune-complex pattern in some renal glomeruli of human SLE patients with lupus proliferative glomerulonephritis but is not detected in normal or pathological control human kidneys. This antigen cross-reacts with p30 interspecies determinants shared by the four chief virus groups and cross-reacts with a partially purified antigen extracted from human SLE spleen. The human SLE spleen antigen cross-reacts with p30 group antigen of RD-114 virus but not of feline or murine viruses. Some host immunoglobulins eluted from a human SLE kidney by acid-buffer show antibody-like activity against p30 group antigen of RD-114 virus but not of simian, feline, or murine viruses.

Animals

Type C RNA virus-specific antibody in human systemic lupus erythematosus demonstrated by enzymoimmunoassay.

Postmortem study of proliferative glomerulonephritis associated with human systemic lumpus has previously shown that an antigen related to mammalian type C RNA viral core (p30) proteins is deposited in the renal glomerular lesions with human immunoglobulins in an immune-complex pattern. In the present work, human immunoglobulins were sequentially eluted from the lupus glomerular immune deposits and were assayed by a sensitive enzymoimmunoassay developed for the measurement of anti-p30 antibody activity against purified viral p30 proteins of mammalian type C viruses. Human immunoglobulins showing specific anti-p30 antibody activity, particularly against p30 antigen of feline endogenous virus RD-114 and to a smaller extent against p30 antigen of murine type C virus, were eluted by acid buffer from the glomerular immune deposits in two patients with lupus proliferative glomerulonephritis who have deposits of viral p30-related antigen in the same tissue lesions. This study adds support for the hypothesis that expression of type C viral antigen may be involved in the multifactorial pathogenesis of proliferative glomerulonephritis associated with human systemic lupus.

Antibodies, Viral

Murine Type C viral envelope glycoprotein gp69/71 and lupus-like glomerulonephritis of New Zealand mice. An immunoperoxidase study.

The location of murine Type C viral envelope glycoprotein antigen in the glomerulonephritic kidneys of NZB and NZB/NZW F1 hybrid mice was analyzed by the indirect immunoperoxidase technique at light and electron microscopic levels. Immune complex deposits of the glycoprotein antigen were present in the glomeruli in mesangial and subepithelial sites. In addition to the glomerular depositions, viral envelope antigen was also present at the brush border of proximal tubular epithelial cells and in lymphoid cells infiltrating the kidneys of these mice.

Animals

The occurrence and frequency of type C virus-like particles in placentas from patients with systemic lupus erythematosus and from normal subjects.

Type C RNA virus-like particles were found by electron microscopy in term placentas from 3 patients with systemic lupus erythematosus (SLE), 1 with probable SLE, and 2 normal patients. The virus-like particles were mainly of a budding or immature type located at or near the cell membrane of syncytiotrophoblasts in chorionic villi. Type C virus-like particles were not observed in the term placenta from a patient with chronic discoid LE, nor in early gestation specimens from 1 normal patient and 4 patients with SLE. The frequency of the Type C particles varied greatly: They were readily found in the patient with probable SLE, and only here were groups of budding particles observed. Type C particles were less numerous in one normal placenta and rare in the other positive placentas, both SLE and normal. Heretofore undescribed crystalline inclusions were found in the cytoplasm of chorionic villous endothelial cells from 3 patients with SLE and 1 with discoid LE. Tubuloreticular structures were observed in the maternal endometrium of 1 patient with SLE.

Chorionic Villi

Electron microscopic study of distinctive structures in peripheral blood lymphocytes obtained from twins with systemic lupus erythematosus.

Peripheral blood lymphoid cells obtained from nine twin pairs (six monozygotic and three dizygotic) in which one or both twins had systemic lupus erythematosus (SLE) were examined by electron microscopy for the occurrence of two distinctive intracytoplasmic structures-tubuloreticular structures (TRS) and tubular crystalloids (TC). TRS were found in 0.8 to 14.8% of lymphoid-cell cross sections in 9 of 11 twins with SLE and 2 clinically well but serologically abnormal twins. Lymphoid cells of twins both clinically and serologically normal did not exhibit TRS, although their monozygotic or dizygotic SLE-positive counterparts possessed these structures. Thus, the expression of TRS was more consistent with an acquired than inborn trait and appeared to correlate with disease and serologic manifestations of SLE. TC were found in 1.7 to 7.9% of lymphoid-cell cross sections in every twin examined. No correlation was recognized between clinical or laboratory data and the frequency of TC-bearing cells. The significance and the ultrastructural development of TC in the peripheral blood lymphoid cells are briefly discussed.

Diseases in Twins

The viral envelope glycoprotein of murine leukemia virus and the pathogenesis of immune complex glomerulonephritis of New Zealand mice.

The use of monospecific antisera for the analysis by radioimmunoassay and immunofluorescence study of two major viral proteins, gp69/71 and p30 of murine leukemia virus, that could be of significance in the pathogenesis of immune complex glomerulonephritis of mice, particularly NZB and B/WF(1) hybrid mice, yielded the following conclusions. A remarkably high concentration of viral envelope glycoprotein, gp69/71, was detected in the spleen and serum of New Zealand mice (NZB, NZW, B/WF(1), and W/BF(1)); the concentration in the spleen was 10-fold greater than that found in AKR mice and 30-fold greater than that present in C57BL/6 mice. The gp69/71 was deposited along with bound immunoglobulins, apparently as an immune complex, in the diseased kidneys of mice, and the glomerular site and extent of deposition of gp69/71 was related to the severity of the glomerulonephritis. This study suggests that the pathogenesis of immune complex glomerulonephritis (and vasculitis) in mice is related to the expression of this specific viral envelope glycoprotein and to the host immune response to this protein.

Animals

Common cell surface antigen associated with mammalian C-type RNA viruses. Cell membrane-bound gs antigen.

The indirect membrane immunofluorescence test and the absorption analysis of rabbit anti-FeLV, rabbit anti-FeLVp 30, and rabbit anti-MuLVp 30 antisera yielded the following conclusions. An antigen shared by mammalian (murine and feline) C-type RNA leukemia and sarcoma viruses was detected on the surface of cells infected or transformed by C-type viruses. The antigen was characterized as membrane-bound gs antigen bearing two determinants, membrane-bound gs-1, intraspecies-specific antigenic determinant, and membrane-bound gs-3, interspecies-specific antigenic determinant. Membrane-bound gs antigen was located on the cell surface, frequently near the site of virus budding but not on the envelope of murine C-type RNA virus.

Animals

Biological expression of antigenic determinants of murine leukemia virus proteins gp69-71 and p30.

Antisera to purified structural proteins of Rauscher murine leukemia virus, the major envelope glycoprotein, gp69/71, and the major internal protein, p30, were studied by immunofluorescence of viable and fixed virus-infected cells and by virus neutralization. Group-specific and type-specific determinants of gp69/71 were demonstrated by immunofluorescence and virus neutralization tests, indicating that these determinants are located in the cytoplasm and probably on the cell surface as well as on virus envelope. Antisera against p30 showed anti-group and anti-interspecies activities by immunofluorescence with no virus-neutralizing activity. Both antigenic determinants of gp69/71 were sensitive to guanidine-hydrochloride and to a lesser degree to ether treatment, whereas the group-specific determinants of p30 were relatively stable to these treatments.

AKR murine leukemia virus

Common cell-surface antigen associated with murine and feline C-type RNA leukemia viruses.

A new common cell-surface antigen associated with murine and feline C-type RNA leukemia viruses was demonstrated by the use of rabbit antiserum against feline leukemia virus and the indirect membrane immunofluorescence test. Common cell-surface antigen was found in all leukemias of all strains of mice tested, in normal lymphoid tissues of Gross-positive (high incidence of leukemia) mouse strains AKR, AKR.H-2(b), C58, and NZB, in cultured rat fibroblasts infected with Rauscher virus, in cultured feline fibroblasts infected with feline leukemia virus, and in spontaneous feline lymphosarcoma. The antigen was not demonstrable in normal adult and fetal tissues of Gross-negative mouse strains or in tissues and cultured fibroblasts derived from normal rats and normal cats. The immunoferritin study of murine leukemia cells revealed that the antigen was located on the cell surface in discrete areas; budding and C-type RNA viral envelope was not labeled as antigen site. The distribution of common cell-surface antigen on murine and feline leukemias, as well as on normal lymphoid tissues of Gross-positive mouse strains, indicates the presence of an antigen distinct from any cell-surface antigen heretofore shown to be associated with, or specified by, mammalian C-type RNA viruses.

Animals