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Biomedical subjects

J G Derge

Publications and source records attributed to J G Derge.

18 recordsLinked to original sources
PubMed1981

Herpes simplex virus (type 1) thymidine kinase gene does not transform cells morphologically.

BALB/c-derived 10E2 cells were made thymidine kinase(TK)-negative and one isolated clone (B2) was used for studying morphological and biochemical transformations by herpes simplex virus (HSV) type 1 (strain 10412). The B2 cells displayed a "normal" flat appearance and were nontumorigenic in nude mice when tested at frequent intervals over a period of 45 subcultures. B2 cells infected with UV-irradiated HSV (UV-HSV) and maintained in normal growth medium showed foci of spindle-shaped cells after one subculture. The cells from these morphologically transformed foci were tumorigenic in nude mice and were TK negative. B2 cells infected with UV-HSV or transfected with the HSV-1 TK gene and maintained in TK-selective medium showed discrete colonies of cells which displayed a normal flat appearance and expressed the viral TK enzyme. These biochemically transformed B2 cells were nontumorigenic in nude mice. The findings with B2 cells indicate that biochemical and morphological transformations by HSV-1 are independent events and suggest that the HSV-1 TK gene is a suitable vehicle for introducing non-TK genes into cells to assess their transforming potential.

Animals↗
PubMed1978

Activation of endogenous type C virus in BALB/c mouse cells by herpesvirus DNA.

Several virion and nonvirion DNAs were tested for the ability to activate endogenous type C virus in BALB/c-derived mouse cells using the calcium precipitation technique. The DNAs from all herpesviruses tested activated xenotropic type C virus synthesis. These included DNAs from herpes simplex virus types 1 and 2, Epstein-Barr virus, human cytomegalovirus, SA8 virus, infectious bovine rhinotracheitis virus, pseudorabies virus, and herpes saimiri virus (M-DNA). In contrast, DNAs from vaccinia virus, simian virus 40, primate cells, bacteria, mycoplasma, and salmon sperm showed no ability to activate type C virus when tested under the same conditions. Several herpesviruses and vaccinia virus, which were highly infectious for the BALB/c cells used, were tested for their ability to activate type C virus after UV irradiation. All herpesviruses tested were positive, while vaccinia virus was negative. Unirradiated simian virus 40 also showed no ability to activate type C virus. Activation of type C virus by DNA from herpes simplex virus was observed after shearing or sonication of the DNA to an average size of 3 x 10(6) daltons, but was not observed with DNA sonicated to an average size of 1 x 10(6) daltons. Alkali denaturation of DNA from herpes simplex virus or treatment with DNase, but not RNase, destroyed its ability to activate type C virus, as did crosslinking of the DNA with 4,5',8-trimethylpsoralen (psoralen) and light.

Cell Line↗
PubMed1976

Activation of an endogenous mouse type C virus by ultraviolet-irradiated herpes simplex virus types 1 and 2.

Infection of BALB/c mouse cells with UV-irradiated herpes simplex virus (HSV) types 1 and 2 resulted in activation of a xenotropic type C virus detected by infectious center formation in permissive rat cells. The levels of type C virus activated by HSV were related to the UV dose and the multiplicity of infection used. The ability of HSV to activate type C virus was eliminated by heat-inactivation and by neutralization with specific antiserum against HSV, but was not affected by purification or treatment with DNase and RNase. Maximum levels of type C virus in the cells and medium were observed within 1 day after HSV infection, and the levels returned to control cell values within 3-4 days. The possible significance of these findings with respect to the putative oncogenic potential of HSV is discussed.

Cell Line↗
PubMed1974

Replication of the resident repressed Epstein-Barr virus genome during the early S phase (S-1 period) of nonproducer Raji cells.

Replication of the resident repressed Epstein-Barr virus genome in synchronized nonproducer Raji cells was shown to occur during the early S phase (S-1 period) by hybridization of cell DNA with virus-specific complementary RNA (cRNA). The S-1 period was previously identified as the critical period for virus activation induced by thymidine analogues. The findings reported here and elsewhere are consistent with the proposal that: (i) virus activation is initiated at or near the site of association of the resident viral genome with cell DNA, (ii) replication of the resident virus genome in nonactivated cells is under cell control mechanisms, and (iii) the resident virus genome is physically associated with early replicating cell DNA.

Burkitt Lymphoma↗
PubMed1972

Protein-polysaccharide biosynthesis. Membrane-bound saccharides.

Membrane-bound saccharides obtained from ear cartilage from rabbits recovering from papain injection were examined for glycosyl acceptor properties, alkali lability, molecular size and degree of sulphation. Although considerable glucuronosyl transfer from UDP-glucuronic acid could be demonstrated, less than one-third could be identified as representing chondroitin linkage formation; there was little or no effect of molecular size on acceptor properties. Approximately one-half of the membrane-associated chondroitin-like saccharide chains are solubilized by alkali, whereas one-half require proteolysis for solubilization. These fractions are analytically indistinguishable and both contain xylose and galactose as well as uronic acid and sulphated N-acetyl-galactosamine. All fragments that were examined contained stoicheiometric amounts of axial sulphate ester, strongly suggesting a close relationship between chain extension and sulphation.

Animals↗
PubMed1972

Synthesis of Epstein-Barr virus after activation of the viral genome in a "virus-negative" human lymphoblastoid cell (Raji) made resistant to 5-bromodeoxyuridine (thymidine kinase-virus antigen-immunofluorescence-herpesvirus fingerprints).

The Raji line of human lymphoblastoid cells, which does not show expression of Epstein-Barr virus, was made resistant to 5-bromodeoxyuridine. Within several weeks after removal of the drug, Epstein-Barr virus particles were detected in the cells. The sequence of virus appearance in the 5-bromodeoxyuridine-resistant cells indicated drug-induced activation of a repressed Epstein-Barr virus genome.

Animals↗
PubMed1972

Sequence of spontaneous Epstein-Barr virus activation and selective DNA synthesis in activated cells in the presence of hydroxyurea.

The sequence of spontaneous Epstein-Barr virus activation was studied in P3HR-1 carrier cells and in P3HR-1(BrdU) cells made resistant to 5-bromodeoxyuridine. Virus activation was initiated during the normal cell cycle, and recruitment of additional virus-activated cells was prevented by the DNA inhibitors, 1-beta-D-arabinofuranosylcytosine and hydroxyurea. Virus activation was followed by synthesis of the early antigen complex in the absence of additional detectable DNA synthesis. Early antigen synthesis was followed by hydroxyurea-resistant synthesis of new DNA, which in the case of P3HR-1(BrdU) cells was characterized by the appearance of thymidine kinase. The newly synthesized DNA banded in neutral cesium chloride at peaks corresponding to normal human DNA and Epstein-Barr viral DNA. Synthesis of viral antigen was seen only in cells that had undergone hydroxyurea-resistant DNA synthesis.

Adenine↗
PubMed1971

Persistence of a repressed Epstein-Barr virus genome in Burkitt lymphoma cells made resistant to 5-bromodeoxyuridine.

The P3HR-1 line of human lymphoblastoid cells that is Epstein-Barr virus positive was made resistant to 5-bromodeoxyuridine. Epstein-Barr virus-associated antigens, but not virus particles, were produced in P3HR-1(BU) cells maintained on 5-bromodeoxyuridine. However, virus particles did appear within 4 days after removal of the drug. Thymidine kinase activity was limited to P3HR-1(BU) cells producing viral antigen, whereas all control P3HR-1 cells showed thymidine kinase activity regardless of viral antigen synthesis. Cellular DNA in most P3HR-1(BU) cells was made via pathways that did not involve thymidine kinase. In cells having a pathway that involved thymidine kinase, a second DNA of density 1.71 g/cm(3), corresponding to Epstein-Barr virus, was detected.IT WAS CONCLUDED THAT: (a) a repressed Epstein-Barr virus genome persists in P3HR-1(BU) cells that do not contain thymidine kinase, with activation of the viral genome being accompanied by productive infection and the appearance of enzyme, and (b) thymidine kinase activity in P3HR-1(BU) cells could be used as a marker for viral genome expression.

Animals↗