Biomedical subjects

S Baron

Publications and source records attributed to S Baron.

At least 217 records · Page 12Linked to original sources

PubMed1975

A modified polyriboinosinic-polyribocytidylic acid complex that induces interferon in primates.

A comlex of polyriboinosinic-polyribocytidylic acid (poly I-poly C) with poly-L-lysine and carboxymethylcellulose has been prepared. This complex is five to 10 times as resistant to hydrolysis by primate serum as the parent poly I-poly C. It has a thermal denaturation temperature about 40 C higher than that of poly I-poly C. The complex induces significant levels of serum interferon in monkeys and chimpanzees under conditions in which poly I-poly C itself induces no interferon.

Animals↗

PubMed1975

Failure of attenuated temperature-sensitive influenza A (H3N2) virus to induce heterologous interference in humans to parainfluenza type 1 virus.

The present investigation was undertaken to determine if a candidate live vaccine virus, influenza A/Hong Kong/68-ts-1 [E] (H3N2), induced heterologous interference against an interferon-sensitive, wild-type, parainfluenza type 1 challenge virus. The parainfluenza virus was administered 7 days after Hong Kong/68-ts-1 [E] virus infection. The clinical response, daily quantitative virus shedding, interferon production, and serum and nasal wash antibody responses were determined in an experimental group (influenza A virus followed by parainfluenza virus) and 10 volunteers in a control group (parainfluenza virus only). The volunteers were selected on the basis of susceptibility to the two viruses, i.e. serum hemagglutination-inhibition antibody titer of is less than or greater to 1:8 for influenza virus and low nasal wash antibody titer (is less than or greater to 1:8) for parainfluenza virus. Despite a 100% infection rate in the Hong Kong/68-ts-1 [E] vaccinees, no heterologous interference was induced against the parainfluenza type 1 virus challenge.

Animals↗

PubMed1975

Murine cytomegalovirus: induction of and sensitivity to interferon in vitro.

Moderate amounts of viral inhibitor were produced by mouse embryo (ME) cultures infected with two strains of plaque-purified murine cytomegalovirus (MCV). This inhibitor was shown to be interferon, based on the possession of similar properties. The growth studies of MCV in ME cells showed that interferon was produced as early as 4 h after infection, infectious virus was produced between 12 to 16 h, and cytopathic effect was produced between 16 to 18 h. Since MCV-induced interferon production and the subsequent development of antiviral state occurred early, the long eclipse period may be due to an interferon-mediated delay of virus replication. Pretreatment of ME cells with varying concentrations of interferon before infection with MCV did not result in increased interferon production, but at high pretreatment doses a slight inhibitory effect on interferon production was observed. In vitro sensitivity studies showed that small doses of MCV were highly sensitive to the antiviral action of interferon, but higher viral doses proved to be markedly resistant. Although the available evidence does not permit a definitive interpretation of the mechanism by which MCV may show differing sensitivities to interferon action, the presence of a small interferon-resistant fraction of virus-infected cells may account for the observations.

Animals↗

PubMed1975

Studies of herpes simplex virus and interferon in human gingival cell cultures.

Cultures of human gingival fibroblast cells from patients with a positive or negative history of recurrent herpes simplex virus (HSV) infection were compared with respect to susceptibility to HSV infection and interferon activity. There was a possible inverse relationship between interferon sensitivity of gingival fibroblast cells and a clinical history of recurrent disease. No correlation was found between prior infection and other parameters of interferon activity or susceptibility of the cells to HSV.

Antibodies, Viral↗

PubMed1975

Inhibitory effect of synthetic polyribonucleotides on the primary in vitro immune response.

The synthetic double-stranded polyribonucleotides, poly (rA):poly (rU) and poly (rI):poly (rC), were shown to be potent inhibitors of the in vitro plaque-forming cell (PFC) response to a thymus-dependent (SRBC) and thymus-independent (E. coli 0127 LPS) antigen in mouse C57BL/6 spleen cell cultures. The same polynucleotides had no effect on the PFC response of nude (athymic) mouse spleen cells to E. coli 0127 LPS, suggesting that functional T lymphocytes are necessary for the inhibitory effect. Enhancement effects were modest and inconsistent in the cultures. Poly (rA) and poly (rU) were ineffective as inhibitors. The data indirectly suggest that the inhibition may be due to the early production of interferon by functional T lymphocytes.

Animals↗

PubMed1975

Absence of detectable interferon in jejunal biopsies, jejunal aspirates, and sera in experimentally induced viral gastroenteritis in man.

Seven of thirteen normal volunteers inoculated with either the Norwalk of Hawaii agent of viral gastroenteritis demonstrated clinical illness, with typical rapid onset, short duration, and rapid recovery. Examination of sera, jejunal aspirates, and jejunal biopsy specimens obtained 48-96 hr after inoculation, failed to reveal the presence of interferon in samples from either ill or well subjects.

Acute Disease↗

PubMed1975

Inhibition of the primary in vitro antibody response by interferon preparations.

The primary in vitro plaque forming cell (PFC) response of mouse (C57BL/6J) spleen cells to sheep red blood cells (SRBC) was inhibited by two sources of crude and two sources of partially purified mouse interferon. The substance(s) in the interferon preparations which induced PFC and antiviral inhibitory activity have the following common characteristics: a) The interferon preparations were of different potencies and specific activities, but they inhibited the PFC response in proportion to their activities; 20 to 60 units were the minimal amounts required for greater than 90% inhibition of the PFC response. b) Both the antiviral activity and the PFC inhibitory activity of the interferons were neutralized by antibody specific for mouse interferon. c) Both activities were partially or completely inactivated by heating at 60 degrees C for 1 h. d) Human interferons had neither antiviral activity nor PFC inhibitory activity in mouse cells. e) Limited exposure (4 h) of cells to interferon significantly inhibits both viral infection and the PFC response. f) Both the antiviral activity and the PFC inhibitory activity of the interferon preparations are acid stable. It is concluded, therefore, that the inhibition of the primary in vitro PFC response is due to interferon in the preparations. Maximum inhibition of the PFC response occurred when interferon was added to cultured at the same time as SRBC. Significant inhibition was also observed when interferon was added 1 day later, and slight enhancement was observed when added at days 2 and 3 of SRBC addition. Kinetic data showed that the greater the concentration of interferon added to the cultures, the earlier the effect on the PFC response. The presence of interferon in cultures for the first 4 h is sufficient to inhibit the PFC response. Interferon, then, appears to affect some early event(s), which leads to inhibition of the PFC response. Since mature T cells can be one of the sources of interferon, we have demonstrated a suppressor effect of a T cell lymphokine. The precise relationship of interferon to various expressions of suppressor T cell effects remains to be determined.

Animals↗

PubMed1974