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M Nonoyama

Publications and source records attributed to M Nonoyama.

At least 109 records · Page 6Linked to original sources
PubMed1985

The structure of Marek disease virus DNA: the presence of unique expansion in nonpathogenic viral DNA.

DNA of Marek disease virus (MDV) consists of two unique regions UL and US flanked by long inverted repeat regions TRL and IRL, and short inverted repeat regions TRS and IRS, respectively, similar to herpes simplex virus DNA. Comparison of restriction patterns between pathogenic and nonpathogenic MDV DNA was made to identify a region of viral DNA different between these two types of MDV, as it may be responsible for the tumorigenicity of MDV in chickens. The results indicated that BamHI-D and -H, located at the long inverted repeat regions TRL and IRL, were specifically expanded in nonpathogenic viral DNA. The location of the expanded region has been determined within 1.5 kilobase pairs of the Bgl I/Pst I fragment of BamHI-D and -H, close to the junction between the inverted repeat and the unique region. The possibility that a gene responsible for tumor induction may be disrupted by such expansion has been discussed.

Animals↗
PubMed1985

Map location of homologous regions between Marek's disease virus and herpesvirus of turkey and the absence of detectable homology in the putative tumor-inducing gene.

The DNA region having homology between Marek's disease virus and herpesvirus of turkey was assigned to the restriction map of Marek's disease virus by Southern blot hybridization. Under moderate conditions at the level of 15% mismatching, homology was found to be distributed throughout the Marek's disease virus genome. The long inverted-repeat regions (TRL and IRL), which are considered to play a significant role in tumorigenicity, did not show any homology to herpesvirus of turkey DNA.

Animals↗
PubMed1984

Identification of Epstein-Barr virus genes expressed during the early phase of virus replication and during lymphocyte immortalization.

Transcription of the Epstein-Barr virus (EBV) genome in Raji cells superinfected with P3HR-1 EBV in the presence of cycloheximide was compared to transcription in human lymphocytes infected with transforming EBV (B95-8). This was done to identify regions of the EBV genome which contain genes that may mediate initiation of virus replication. Hybridization of 32P-labeled cDNA to cloned fragments of EBV DNA (dot blot hybridization) was employed to identify transcriptionally active regions of the viral genome in these cells. DNA in the BamHI A, F, H, and M restriction fragments was found to encode poly(A) RNA during the early phase of EBV replication. In the absence of cycloheximide the earliest detectable transcripts were transcribed from the BamHI M region. The most transcriptionally active region of the EBV genome in lymphocytes following infection with EBV (B95-8) was the BamHI W-Y-H-F region and, to a lesser extent, the K region. Transcription of the BamHI M region was not detected in these cells. The data suggest that expression of a gene or genes located in the BamHI M region of the EBV genome is an important event in the initiation of EBV replication, whereas expression of the genes in the BamHI W-Y-H-F and K regions may be important in the establishment of latency and cellular immortalization.

Cells, Cultured↗
PubMed1984

Structure of Marek's disease virus DNA: detailed restriction enzyme map.

Purified virion DNA (120 X 10(6) molecular weight [MW]) of Marek's disease virus strain GA was cleaved with BamHI restriction endonuclease, and 27 out of the 29 fragments were cloned into bacterial plasmids. Restriction maps for BamHI, BglI, and SmaI endonucleases were constructed. The genomic structure of Marek's disease virus DNA was found to be similar to that of herpes simplex virus types 1 and 2. A long unique region (75 X 10(6) MW, located at 10 X 10(6) to 85 X 10(6) MW [10-85] from the left end of the genome), which was subdivided into segment 1 (22 X 10(6) MW, located at 10-32) and segment 2 (51 X 10(6) MW, located at 34-85) by direct repeats (32-34), was flanked by a long terminal region (10 X 10(6) MW, located at 0-10) and a long inverted region (10 X 10(6) MW, located at 85-95). A short unique region (8 X 10(6) MW, located at 103-111) was flanked by a short terminal region (8 X 10(6) MW, located at 111-119) and a short inverted region (8 X 10(6) MW, located at 95-103). The direct repeat fragments (0.9 X 10(6) could be isolated by cleavage with SmaI. The right terminal end was found to be heterogenous .

Animals↗
PubMed1984

Lymphoblastoid cell-induced suppression of human peripheral blood leukocyte mitogenic responses.

Two lymphoblastoid tumor cell lines, the Burkitt lymphoma derived BJAB cell line which is free of Epstein-Barr virus (EBV) and B95-8 cells, which are marmoset lymphocytes transformed by EBV isolated from an infectious mononucleosis patient, were studied in regards to their effects on the blastogenic responsiveness of normal human peripheral blood leukocytes stimulated in vitro with mitogens. Mitomycin C treated tumor cell suspensions, when cocultured with normal human blood leukocytes, markedly depressed the expected blastogenic responses in vitro to concanavalin A, pokeweed mitogen, and phytohemagglutin. In addition, cell-free sonicates from the cell lines also depressed blastogenic responsiveness of the leukocytes in vitro. Heating the sonicates for 10 min at 100 degrees C markedly diminished the suppressive properties of the sonicates, as did ultraviolet light irradiation. The suppressive activity of the B95-8 sonicates was pelleted by high speed centrifugation as compared to the activity of sonicates derived from the BJAB cells. Further studies are warranted to determine the nature and mechanism of suppression of blastogenic responsiveness of normal human leukocytes by soluble components derived from such lymphoblastoid cell lines.

Animals↗
PubMed1983

Transcription of the Epstein-Barr virus genome in productively infected cells.

Transcription of the genome of Epstein-Barr virus in productively infected B95-8 cells was studied. Dot blot hybridization of cDNA prepared from cytoplasmic viral poly(A)RNA with 28 different cloned BamHI fragments of EBV DNA indicated that the patterns of viral genome transcription were similar in control and TPA-treated cells. However, three fragments, BamHI I, R, and Z, appeared to be newly induced in TPA-treated cells, as no significant level of transcription of these fragments was observed in control cells. In contrast, there was no detectable transcription from fragments BamHI P, a, and b even in cells treated with TPA. The size of virus-specific RNA was determined by agarose gel electrophoresis followed by Southern blot hybridization using radioactive BamHI cloned EBV DNA fragments as probes. Sixty-eight cytoplasmic poly(A)RNA species, ranging in size from 0.1 to 2.8 megadaltons, were detected by this procedure.

Animals↗
PubMed1983

Phosphonoacetic acid-resistant RNA of Epstein-Barr virus in productively infected cells.

The transcription of Epstein-Barr virus genome in productively infected B95-8 cells in the presence or absence of phosphonoacetic acid (PAA) was studied. Twenty-eight species of cytoplasmic poly(A)-containing virus mRNA were identified as PAA resistant. Some of these viral mRNAs were not detected in the absence of PAA. The most actively transcribed fragments of cloned EBV DNA in the presence of PAA were BamHI H (map unit 29.1-32.5) and M (47.3-50.3). The treatment of TPA-induced B95-8 cells with cycloheximide abolished most cytoplasmic viral poly(A) RNAs, and only three species of viral mRNA (0.7, 1.0, and 1.6 megadaltons) were detectable by hybridization with the BamHI M fragment.

Animals↗
PubMed1983

A search for rheumatoid arthritis-associated nuclear antigen and Epstein-Barr virus specific antigens or genomes in tissues and cells from patients with rheumatoid arthritis.

Pannus extracts and/or cells and tissues from rheumatoid arthritis (RA) patients and controls were tested for the presence of RA-associated nuclear antigen (RANA), anti-RANA, Epstein-Barr virus (EBV)-specific antigens, and EBV genomes. Using our present rather insensitive methods, RANA was rarely detected in RA pannus extracts or tissues, whereas anti-RANA was commonly found. EBV-specific antigens or genomes could not be detected in a limited number of tissues tested using our present methods. The data suggest that EBV may not be the primary event causing RA through direct infection and transformation of synovial tissues.

Antibodies, Antinuclear↗
PubMed1982

Partial restriction map of Marek's disease virus DNA.

A partial restriction map of Marek's disease virus (MDV) DNA was constructed by digestion with endonucleases BamHI, Bg/I and SmaI and by blotting hybridization. The data suggest that there is a terminal heterogeneous sequence at least on one end of the MDV DNA molecule. The data did not reveal four different orientations of the terminal fragments of MDV DNA molecules despite the observation that MDV DNA contains inverted repeat sequences as also present in Herpes simplex virus (HSV) DNA molecules (Cebrian et al., 1981). Terminal deletion of MDV DNA, SalI-H and I, was found in high passage number preparations.

Animals↗
PubMed1981

Epstein-Barr virus-induced malignant lymphoma in a white-lipped marmoset.

One of six white-lipped marmosets inoculated with cell-free B95-8 virus developed diffuse malignant lymphoma. Epstein-Barr virus (EBV) DNA was detected in a pathologically enlarged mandibular lymph node by DNA-DNA hybridization. The affected animal at the time of killing had EBV antibody titers of 1:320 for viral capsid antigen (VCA) and 1:20 for early antigen (EA) while all non-diseased animals had less than or equal to 1:80 VCA antibody and no detectable EA antibody. This is the first report of lymphoma development in a white-lipped marmoset following EBV inoculation.

Animals↗
PubMed1981

Cloning of Epstein-Barr virus (EBV) DNA fragments in pBR32 and Charon3A.

Restriction fragments of Epstein-Barr virus (EBV; B95-8) DNA were cloned in the Tc gene of pBR322 (HindIII-F, -G, -I, -J, -K, -L, and -M) and in Charon3A (EcoRI-GI and -G2). Altogether these cloned fragments covered 39% of the entire viral genome. The cloned EcoRI-G2 fragment of EBV (B95-8) DNA was shown to contain, in addition to HindIII-J, two more HindIII-fragments : HindIII-M, which had not been located on the linkage map of the viral genome (Given and Kieff, 1978) and HindIII-N, which had been unrecognized up to now. The utility of this cloning method is discussed in regard to the detailed mapping of a viral genome and large-scale production of the viral DNA.

Bacteriophage lambda↗
PubMed1981

Linkage map of the fragments of herpesvirus papio DNA.

Herpesvirus papio (HVP), an Epstein-Barr-like virus, causes lymphoblastoid disease in baboons. The physical map of HVP DNA was constructed for the fragments produced by cleavage of HVP DNA with restriction endonucleases EcoRI, HindIII, SalI, and PvuI, which produced 12, 12, 10, and 4 fragments, respectively. The total molecular size of HVP DNA was calculated as close to 110 megadaltons. The following methods were used for construction of the map; (i) fragments near the ends of HVP DNA were identified by treating viral DNA with lambda exonuclease before restriction enzyme digestion; (ii) fragments containing nucleotide sequences in common with fragments from the second enzyme digest of HVP DNA were examined by Southern blot hybridization; and (iii) the location of some fragments was determined by isolating individual fragments from agarose gels and redigesting the isolated fragments with a second restriction enzyme. Terminal heterogeneity and internal repeats were found to be unique features of HVP DNA molecule. One to five repeats of 0.8 megadaltons were found at both terminal ends. Although the repeats of both ends shared a certain degree of homology, it was not determined whether they were identical repeats. The internal repeat sequence of HVP DNA was found in the EcoRI-C region, which extended from 8.4 to 23 megadaltons from the left end of the molecule. The average number of the repeats was calculated to be seven, and the molecular size was determined to be 1.8 megadaltons. Similar unique features have been reported in EBV DNA (D. Given and E. Kieff, J. Virol. 28:524-542, 1978).

Animals↗
PubMed1980

Mitogenic effect of 12-0 tetradecanoyl phorbol 13-acetate on non-human primate mononuclear cells and in vitro interaction with Epstein-Barr virus transformation.

12-0 tetradecanoyl phorbol 13-acetate (TPA), known to promote tumors in mice and also to enhance viral transformation as well as induction of viral antigens, was demonstrated to be mitogenic to peripheral blood mononuclear cells from rhesus monkeys and three species of marmosets. Even though mitogenic responses varied between species and within species, the mitogenic dose response due to TPA was comparable to the response of phytohemagglutinin (PHA-P). A significant synergistic effect of PHA-P and TPA on mononuclear cells from marmosets was evident when they were used together at optimal doses. TPA also increased the efficiency of in vitro transformation of marmoset lymphocytes by Epstein-Barr virus.

Animals↗
PubMed1980

Human nasopharyngeal carcinomas positive for Epstein-Barr virus DNA in North America.

Nasopharyngeal carcinomas (NPC) from 2 black patients and 1 Caucasian patient were positive for Epstein-Barr virus (EBV) DNA. Of the tumors, 2 were lymphoepitheliomas (undifferentiated NPC) and 1 was a moderately differentiated NPC. All 3 patients had high IgG titers against EBV early antigen and high IgG and IgA titers against virus capsid antigen (VCA). In one patient, the levels of anti-VCA IgA were different than those of anti-VCA IgG over the course of the disease. Our data support the association of EBV and NPC in North America.

Adolescent↗