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N B Raj

Publications and source records attributed to N B Raj.

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Nuclear ribonucleoprotein complexes containing U1 and U2 RNA.

Nuclear ribonucleoprotein (RNP) complexes that contain the U1 and U2 RNA of chromatin of Novikoff hepatoma cells were extracted with 0.01 M Tris-HCl (pH 8.0) after the nuclei were initially washed with 0.075 M NaCl and 0.025 M EDTA (pH 8.0). These RNP complexes were purified by chromatography on Sepharose 6B columns and centrifugation on sucrose density gradients. The identity of the U1 and U2 RNA in these particles was established by their electrophoretic mobility in polyacrylamide gels and their T1 RNase fingerprints which were identical with those of authentic U1 and U2 RNA (R. Reddy et al. (1974), J. Biol. Chem.249, 6486-6494; H. Shibata et al. (1974), Mol. Cell. Biochem. 4, 3-19). The nuclear riboncleoproteins had a buoyant density of 1.47 g/ml in CsCl gradients. Two-dimensional polyacrylamide gel electrophoresis of their proteins showed these RNP complexes contain 10 polypeptide spots, of which two are phosphorylated in vivo.

Animals↗

Herpes simplex virus type-1 can reactivate transcription of latent human immunodeficiency virus.

The human immunodeficiency virus, HIV (formerly T-cell lymphotropic virus type III, HTLV-III or lymphadenopathy-associated virus, LAV) is the primary cause of AIDS (acquired immune deficiency syndrome). Patients with AIDS have profound immunosuppression as a result of almost complete absence of the OKT4+ cell population and are predisposed to a number of opportunistic infections as well as to certain malignant diseases such as Kaposi's sarcoma and B-cell tumours. The majority of the opportunistic infections observed in AIDS patients are from the herpesvirus group and these are frequently the cause of death in AIDS patients. We have therefore investigated the effect of herpes virus infection on the expression of HIV and we provide evidence that herpes simplex virus type I (HSV-I) can reactivate transcription of latent HIV. In OKT4+ human T-cells HIV replicates to high virus titres, resulting in high level expression of viral RNA. This high level of expression has been attributed to virus-associated trans-acting factors that increase gene expression, directed by the HIV long terminal repeats (LTR), post-transcriptionally. In our studies we have tested whether transcription directed by the LTR of HIV is stimulated by HSV-I.

Antibodies, Monoclonal↗