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Biomedical subjects

J L Melnick

Publications and source records attributed to J L Melnick.

At least 361 records · Page 20Linked to original sources
PubMed1968

Variation in the oncogenic potential of human adenoviruses carrying a defective SV40 genome (PARA).

The acquisition of the defective SV40 genome by a variety of human adenovirus serotypes by the process of transcapsidation has resulted in the addition of oncogenic potential for newborn hamsters to the previously nononcogenic adenovirus types 1, 2, 5, and 6. These serotypes have previously been grouped together by the high GC content of their DNA. Transcapsidation of the SV40 genome to weakly oncogenic adenovirus types 3, 14, 16, and 21 has failed to increase their oncogenic potential although the parent adenovirus type 7 carrying PARA is highly oncogenic. These serotypes belong to the group possessing a DNA of intermediate GC content. All the PARA-adenovirus populations, even those that were nononcogenic, were able to induce SV40 transplantation immunity and therefore carry the SV40 transplantation marker as well as the marker for synthesis of SV40 tumor or T antigen.

Adenoviridae↗
PubMed1968

Adeno-associated satellite virus interference with the replication of its helper adenovirus.

Adeno-associated satellite virus type 4 interferes with the replication of its helper adenovirus. No interferon-like soluble substance could be detected in satellite-infected cultures and other DNA- and RNA-containing viruses were not inhibited by coinfection with satellite virus under conditions which reduced adenovirus yields by more than 90% in monkey cells. Altering the concentration of adenovirus in the presence of constant amounts of satellite resulted in a constant degree of interference over a wide range of adenovirus inocula and suggested that adenovirus concentration was not a significant factor in the observed interference. The interference with adenovirus replication was abolished by pretreating satellite preparations with specific antiserum, ultraviolet light or heating at 80 degrees C for 30 min. This suggested that infectious satellite virus mediated the interference. Satellite virus concentration was found to be a determinant of interference and studies indicated that the amount of interference with adenovirus was directly proportional to the concentration of satellite virus. 8 hr after adenovirus infection, the replication of adenovirus was no longer sensitive to satellite interference. This was true even though the satellite virus was enhanced as effectively as if the cells were infected simultaneously with both viruses. Interference with adenovirus infectivity was accompanied by reduced yields of complement-fixing antigen and of virus particles which suggested that satellite virus interfered with the formation and not the function of adenovirus products. When cells were infected either with adenovirus alone or with adenovirus plus satellite, the same proportion of cells plated as adenovirus infectious centers. However, the number of plaque-forming units of adenovirus formed per cell in the satellite-infected cultures was reduced by approximately 90%, the same magnitude of reduction noted in whole cultures coinfected with satellite and adenovirus. This suggested that all cells infected with the two viruses were producing a reduced quantity of adenovirus.

Adenoviridae↗
PubMed1968

Efficient filtration and sizing of viruses with membrane filters.

Untreated membrane filters retain viruses by adsorption, as well as by physical restriction which occurs when the pore diameter of the filter is smaller than that of the virus particle. As originally recommended by Elford, membranes had to be pretreated with proteinaceous material to preclude virus adsorption. However, coating materials that prevent adsorption of certain viruses do not necessarily prevent adsorption of other viruses. In contrast to proteins, salts enhance virus adsorption. Viruses treated with sodium lauryl sulfate to reduce the surface tension, or purified viruses in distilled water, are not adsorbed to membranes. A procedure is recommended by which viruses may be passed through membranes with a porosity twice the diameter of the virus. Such filtrates, which contain 50 to 100% of the initial virus concentration, should be used for sizing viruses by subsequent filtration through smaller pores. The determination of virus size would then be based on the major population of particles in the virus suspension. In the past, as little as 0.1 to 0.001% of the initial virus population was the basis for size determination, because more than 99.9% of the virus was often lost by adsorption to membranes during the clarifying procedures.

Adsorption↗
PubMed1968

Defectiveness of interferon production and of rubella virus interference in a line of African green monkey kidney cells (Vero).

Vero cells, a line of African green monkey kidney cells, failed to produce interferon when infected with Newcastle disease, Sendai, Sindbis, and rubella viruses, although the cells were sensitive to interferon. Further, infection of Vero cells with rubella virus did not result in interference with the replication of echovirus 11, Newcastle disease virus, or vesicular stomatitis virus, even in cultures where virtually every cell was infected with rubella virus. Under the same conditions, BSC-1 cells and other cells of primate origin produced interferon and showed rubella virus interference. The results indicate that the presence of rubella virus in the cell does not in itself exclude multiplication of other viruses and that rubella virus interference appears to be linked to the capability of the cell to produce interferon.

Animals↗
PubMed1968

Mechanism of enhancement of virus plaques by cationic polymers.

It has been assumed that plaque enhancement by cationic polymers is due to their binding of sulfated polysaccharides in agar. However, viruses that are enhanced by cationic polymers, diethylaminoethyl-dextran, and protamine were found not to be inhibited by polyanions in agar under the usual overlay conditions. In the case of adenovirus, enhancement by protamine seems to be due to the protamine serving as a source of arginine; enzymes released from the cultured cells digest the protamine and provide a reservoir of arginine for the cells. Other viruses (herpes and echovirus types 3, 4, 5, and 6) known to be susceptible to agar inhibitors were found to be enhanced by cationic polymers even under starch gel and methylcellulose overlays, which are free of polyanions. Since cationic polymers enhance the diffusion of virus through agar or starch gel, plaque enhancement seems to be the result of the gel becoming positively charged so that viruses can move effectively through them. The observation that starch gel and methylcellulose enhance plaque formation with viruses known to be inhibited under agar was also reinvestigated. When the consistency of the agar gel was reduced to the same viscosity of starch gel and methylcellulose overlays, the same plaque counts and sizes were observed under all three overlays.

Adenoviridae↗
PubMed1968

WHO collaborative studies on enterovirus reference antisera: second report.

This paper summarizes the results of the second part of co-operative studies undertaken by the WHO International Reference Centre for Enteroviruses and a number of WHO Regional Virus Reference Centres, WHO Virus Collaborating Laboratories and other laboratories in a comprehensive testing programme of enterovirus equine antisera. The studies were designed to appraise the specificity of immune serum prepared in horses against 16 representative prototype enteroviruses (polioviruses 2 and 3, coxsackieviruses A7, B1, B2, B4, B5 and B6 and echoviruses 1, 2, 3, 5, 7, 9, 12 and 17). Tests for neutralizing antibody were performed not only against the homologous viruses but also against the homotypic strains available in each laboratory. Tests for heterotypic antibody were made against the entire group of enteroviruses, reoviruses 1-3 and adenoviruses 1-11, 13 and 17. Each serum sample represented a pool of the individual bleedings taken from a group of horses before and after immunization with each virus antigen. The results showed that the homologous geometric mean titres of the immune sera ranged from 7000 to 36 000, whereas the preinoculation sera were negative. Results of the homotypic tests showed the usefulness of the sera. The specificity of the haemagglutination-inhibiting antibody of the sera against coxsackieviruses A7, B1, B5, B6 and echoviruses 3, 7, 12 was demonstrated. The results of the tests performed in tissue culture and mice are discussed. Co-operative testing of other enterovirus equine antisera is now in progress.

Animals↗