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Biomedical subjects

S Baron

Publications and source records attributed to S Baron.

At least 199 records · Page 11Linked to original sources
PubMed1977

The transfer of interferon-induced viral resistance between animal cells.

In summary we have shown that interferon treated mouse L cells can transfer their antiviral resistance to cocultured heterologous (human WISH or hamster BHK) cells which are insensitive to mouse interferon. Transfer of viral resistance seems to be initiated by interferon itself. Once transferred the viral resistance has the characteristics of the interferon-induced antiviral state. The transferred resistance occurs between several cell species. The transfer of resistance depends on the ratio of cells homologous (to interferon) to cells which are heterologous as well as to the absolute cell density at a given ratio. The transfer process is efficient in that it requires relatively small amounts of interferon. Finally, we propose that this phenomenon is a natural process for amplification of the interferon system and preliminary evidence indicates that it occurs by cell to cell transfer of an interferon-induced molecule.

Animals↗
PubMed1976

Prophylactic control of simian hemorrhagic fever in monkeys by an interferon inducer, polyriboinosinic-polyribocytidylic acid-poly-L-lysine.

A nuclease-resistant complex of polyriboinosinic-polyribocytidylic acid containing poly-L-lysine and carboxymethylcellulose was used as prophylactic treatment of simian hemorrhagic fever in rhesus monkeys. This infection has proven uniformly fatal to more than 50 monkeys. Treatment 8 hr before infection and repeatedly thereafter completely prevented the development of viremia and death. Untreated animals died before development of antibodies to the virus. None of the treated animals developed antibody to the virus, a fact which suggested that viral growth was essentially completely blocked by the compound.

Animals↗
PubMed1976

A phase I-II trial of multiple-dose polyriboinosic-polyribocytidylic acid in patieonts with leukemia or solid tumors.

Polyriboinosinic-polyribocytidylic acid (poly I - poly C), an interferon inducer, was administered in multiple doses of 0.3-75 mg/m2 to 26 patients with a variety of solid tumors, 9 with acute leukemia, and 2 with chronic myelogenous leukemia in blast crisis. Forty-four separate drug trials were comprised of various schedules and routes of administration. Toxic reactions included fever (in 66% of the trials), transient elevation of serum glutamic-oxaloacetic transaminase and serum glutamic-pyruvic transaminase (25%), minimal laboratory evidence of coagulation abnormalities (59%), and hypersensitivity (5%). These toxic manifestations did not relate to dose level or magnitude of interferon induction. Poly I - poly C administered iv induced low serum concentrations of interferon in 24/38 trials (63%), but the correlation between drug dose and peak interferon titer was not linear. Poly I - poly C administered iv or im was not effective as an inducer of interferon in the cerebrospinal fluid. Similarly, poly I - poly C administered im or by inhalation did not produce detectable serum levels of interferon. No patients experienced an objective tumor response to the administration of poly I - poly C, and most (76%) had progression of their disease while receiving the drug.

Acute Disease↗
PubMed1976

Comparative production of interferon by explanted lymphoreticular tissue and alveolar macrophages from rabbits and humans.

Studies were undertaken to compare interferon production among a variety of lymphoreticular cells, with emphasis on the alveolar macrophage. Explanted cells from rabbit lung, spleen, peritoneum, bone marrow, and blood produced interferon in varying amounts in response to six of the seven viruses studied. The various lymphoreticular tissues responded differently to a single interferon-inducing virus, and each tissue produced varying amounts of interferon when stimulated by different viruses. In addition, glass-adherent rabbit alveolar macrophages produced more interferon than did the nonadherent subpopulation. Human blood and lung cells produced much less interferon than did the equivalent rabbit cells under similar conditions of stimulation. It appeared that interferon production may have been controlled by several variables, including the species, the type of inducer, and the type of tissue and cell.

Adult↗
PubMed1976

Three strains of influenza A virus (H3N2): interferon sensitivity in vitro and interferon production in volunteers.

Three antigenic variants of the H3N2 subtype of wild-type influenza A virus (representing the years 1968, 1972, and 1974) were examined for their sensitivity to interferon and for their ability to induce local respiratory tract interferon in volunteers. In addition, the time of appearance of symptoms in infected volunteers was correlated with the patterns of virus shedding and interferon production. The sensitivity to interferon and the ability to stimulate nasopharyngeal interferon were similarly high for all three strains. Symptomatic illness, peak virus shedding, and peak interferon response all occurred within a 26-h period. These findings imply that interferon or its inducers theoretically could be protective if applied prophylactically, but would be less efficacious when used therapeutically.

Adult↗
PubMed1976

Vesicular stomatitis virus plaque production in monolayer cultures with liquid overlay medium: description and adaptation to a one-day, human interferon-plaque.

Vesicular stomatitis virus forms discrete, microscopic plaques in stationary cultures of the WISH amnion cell line. Microplaque formation is rapid, reproducible, and easily quantitated, occurs at temperatures ranging from 33 to 40 degrees C, and does not require a semisolid overlay. WISH cells, however, are less sensitive to vesicular stomatitis virus than are chicken embryo, 3T6, or Vero cells. WISH amnion cells also are highly sensitive to the antiviral effects of human interferon, and a quantitative human interferon assay, based on vesicular stomatitis virus plaque reduction in WISH cells, is described. This interferon assay can be performed within 1 day, uses a liquid overlay medium, does not require a vital stain, is as sensitive as other methods that use diploid cell strains, and is performed in a microtiter system.

Cell Line↗
PubMed1976

Interferon: effects on the immune response and the mechanism of activation of the cellular response.

The discovery of interferon in 1957 by Drs. Isaacs and Lindenmann led to major revisions in the concepts of man's defenses against viral infections. There are at least two types of interferon. Along with their antiviral properties, they have recently been shown to exert a suppressive effect on the humoral and cellular immune response; they affect both B and T lymphocytes. A variety of substances, including virus, polyribonucleotides, and mitogens for T lymphocytes, are good interferon inducers. T lymphocytes seem to be necessary for these inducers to exert their immunosuppressive effects. The immunosuppressive effects of interferon inducers suggests that interferons may be mediators of suppressor T lymphocyte effects. In the virus system, interferon does not exert its antiviral effects by direct action on the virus, but rather derepresses a cell gene that results in the production of an antiviral protein. This antiviral protein is probably the mediator of inhibition of virus replication. This is a complex sequence of events that results in the interaction of interferon with the cell membrane and the resulting production of the antiviral state in the cell. This review will examine the various steps of this involved process.

Animals↗
PubMed1976

Kinetics of the rapid action of interferon.

The present study was undertaken to examine some factors which lead to early-appearing resistance in human cells treated with interferon. It was previously shown that two conditions required for rapid development of resistance were continuous maintenance of cultures at 37 degrees and use of more than 10 units/ml of interferon. The decay kinetics of the established resistance appear to be approximately the same whether the resistance was induced under conditions favoring rapid or slow development. With the use of actinomycin D it was shown that the mRNA for the antiviral protein is produced between 30 and 45 min after the first contact with interferon. Ruled out were the possibilities that a priming action of interferon and a newly synthesized intermediary protein were necessary for rapid development of resistance.

Cycloheximide↗