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Biomedical subjects

B Hampar

Publications and source records attributed to B Hampar.

At least 55 records · Page 3Linked to original sources
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↗
PubMed1971

Serologic evidence that a herpes-type virus is the etiologic agent of heterophile-positive infectious mononucleosis.

The antibody activity against herpes-type virus (HTV) of heterophile-positive infectious mononucleosis sera and "normal" sera from humans was determined with immunoferritin. The antiviral activity of the mononucleosis sera was associated with the IgM antibodies, while the antiviral activity of the "normal" human sera was associated with the IgG antibodies. It was concluded from these findings that the appearance of antibodies to herpes-type virus in heterophile-positive sera represents a primary immunogenic exposure to this virus, or to a serologically related virus. This conclusion, in turn, suggests that herpes-type virus or a serologically related virus is the etiologic agent of heterophile-positive mononucleosis.

Adolescent↗