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Biomedical subjects

S E Grossberg

Publications and source records attributed to S E Grossberg.

102 records · Page 6Linked to original sources
PubMed1966

Exaltation of the development of poliovirus by semicarbazide.

Grossberg, Sidney E. (Institut Pasteur, Paris, France), Marguerite Lwoff, and André Lwoff. Exaltation of the development of poliovirus by semicarbazide. J. Bacteriol. 92:1473-1477. 1966.-Semicarbazide (NH(2)-NH-CO-NH(2)) remarkably increases the development of poliovirus. In single-cycle experiments, semicarbazide (SCZ) acted to (i) diminish the length of the latent period, (ii) increase the rate of production of virions, and (iii) increase the final yield of virus. These effects were demonstrable in KB cells, a human malignant cell line, and other primate cells. The dose range over which the compound exerts its effect was relatively large, i.e., from 0.3 to 20 mm, whereas higher concentrations inhibited viral growth. SCZ achieved its exalting effect only when it was added during the first 3 hr of viral development; later addition had no effect. Withdrawal of SCZ at intervals during the viral cycle confirmed that its action occurred within 3 hr after infection. The possible mode of action of SCZ is discussed. SCZ appeared to act, at least in part, by increasing the rate of synthesis of the viral ribonucleic acid.

Humans↗
PubMedDate not supplied

A human B-lymphoblastoid cell line constitutively producing Epstein-Barr herpesvirus and JHK retrovirus.

The human B-lymphoblastoid cell line, designated JHK-3, with pre-B-cell characteristics, chronically produces two viruses, Epstein-Barr virus (EBV) and JHK virus, an apparently novel retrovirus. The JHK-3 cells are much more productive of extracellular EBV than the high-producer marmoset line B95-8. The extracellular virus of the JHK-3 EBV strain is relatively fragile, more broadly dispersed in an ultracentrifuged sucrose gradient than the B95-8 EBV and more susceptible to disruption by combined treatment with urea and dithiothreitol. By restriction fragment length polymorphism analysis, the JHK-3 EBV strain resembles the EBV strain FF-41. The JHK-3 cells also produce an incompletely characterized, relatively fragile, enveloped, icosahedral RNA virus that contains Mn(++)-dependent reverse transcriptase. JHK virions measure 85 nm in ultrathin sections, much smaller than other Retroviridae. The JHK virus exhibits a distinctive morphogenesis, most nearly resembling C-type retroviruses. The JHK-3 cell line provides a human cell model for investigating virus/virus interactions and their pathogenetic affects on host cells which chronically and simultaneously produce DNA and RNA viruses.

Animals↗
PubMedDate not supplied

Inhibition of the differentiation of 3T3-L1 cells by interferon-beta and difluoromethyl ornithine.

Both mouse interferon-beta (MuIFN-beta) and the inhibitor of ornithine decarboxylase (ODC), alpha-difluoromethyl ornithine (DFMO), inhibited the differentiation of mouse 3T3-L1 fibroblasts into adipocytes in a dose-dependent manner. DFMO and MuIFN-beta added together to cultures that were induced to differentiate produced an additive anti-differentiation effect. In contrast to this additive cellular effect, DFMO reduced the antiviral activity of MuIFN-beta in both undifferentiated and differentiated cells; DFMO alone had no detectable effect on replication of encephalomyocarditis virus. Putrescine, the product of ornithine decarboxylation, when added to 3T3-L1 cultures (i) enhanced differentiation, (ii) reversed completely the inhibition of differentiation by DFMO, but (iii) had little effect on the antidifferentiation effect of MuIFN-beta. Polyamine content changed four-fold or less in cultures treated with 0.5 mM DFMO and less than two-fold in cultures treated with 100 IU/ml MuIFN-beta for seven days. Thus, it appears not only that MuIFN-beta and DFMO inhibit differentiation of 3T3-L1 cells by different mechanisms but also that the antiviral action of IFN does not involve the regulation of polyamine metabolism by ornithine decarboxylase.

Adipose Tissue↗
PubMedDate not supplied

Inhibition of the differentiation of 3T3-L1 cells by interferon-beta and difluoromethyl ornithine.

Both mouse interferon-beta (MuIFN-beta) and the inhibitor of ornithine decarboxylase (ODC), alpha-difluoromethyl ornithine (DFMO), inhibited the differentiation of mouse 3T3-L1 fibroblasts into adipocytes in a dose-dependent manner. DFMO and MuIFN-beta added together to cultures that were induced to differentiate produced an additive anti-differentiation effect. In contrast to this additive cellular effect, DFMO reduced the antiviral activity of MuIFN-beta in both undifferentiated and differentiated cells; DFMO alone had no detectable effect on replication of encephalomyocarditis virus. Putrescine, the product of ornithine decarboxylation, when added to 3T3-L1 cultures (i) enhanced differentiation, (ii) reversed completely the inhibition of differentiation by DFMO, but (iii) had little effect on the anti-differentiation effect of MuIFN-beta. Polyamine content changed four-fold or less in cultures treated with 0.5 mM DFMO and less than two-fold in cultures treated with 100 IU/ml MuIFN-beta for seven days. Thus, it appears not only that MuIFN-beta and DFMO inhibit differentiation of 3T3-L1 cells by different mechanisms but also that the antiviral action of IFN does not involve the regulation of polyamine metabolism by ornithine decarboxylase.

Animals↗
PubMedDate not supplied

Approaches to the stabilization of interferons.

Considerable effort has been expended in the past few years toward establishing an armamentarium of different techniques to stabilize naturally produced alpha-and beta-interferons, particularly the beta type in view of its greater lability. Of the techniques reported, it seems that addition of various proteins, rare earth salts, and use of acid pH conditions may be the most useful since they are relatively nontoxic and protect against both thermal and mechanical stress inactivation. Little has so far been reported on the stability of recombinant DNA-derived interferons. It is unlikely that they will be any more stable when they are purified than the natural human interferons. To generate stable preparations of these bacteria-produced interferons for clinical use it is important to establish different nontoxic techniques and approaches to prevent inactivation of these interferons during preparation, processing, concentration, purification and storage.

Clinical Trials as Topic↗