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Biomedical subjects

I Gresser

Publications and source records attributed to I Gresser.

At least 163 records · Page 9Linked to original sources
PubMed1978

Role of interferon in the pathogenesis of viral diseases of mice as demonstrated by the use of anti-interferon serum. V. Protective role in mouse hepatitis virus type 3 infection of susceptible and resistant strains of mice.

Potent sheep anti-mouse interferon globulin has been used to determine the role of virus-induced interferon in mouse hepatitis virus type 3-infected susceptible (C57BL/6), semiresistant (C3H/He), and resistant (A/J) strains of mice. Injection of anti-interferon globulin accelerated the onset of death in C57BL/6 mice, induced almost 100% mortality in C3H/He mice that usually do not die of acute disease, and caused death in 4- and 6-week-old A/J mice, but not in older mice. We conclude that interferon is an important host defense factor in the initial response of different strains of mice to MHV-3 infection. Other factors, however, such as the capacity of macrophages to restrict viral multiplication probably underlie the genetically determined susceptibility or resistance of mice to MHV-3 infection.

Animals↗
PubMed1978

Role of interferon in the pathogenesis of herpes simplex virus disease in mice.

The use of a potent antiinterferon serum has demonstrated the importance of the interferon response in host resistance to infection with herpes simplex virus (HSV). Inoculation of mice with potent antiinterferon globulin was associated with a very marked effect on the evolution of HSV disease, as shown by an acclerated appearance of signs of disease and death. In a total of seven experiments, i.v. administration of a sheep antimouse interferon globulin (titre 4 x 10(5)) resulted in the early appearance of disease and death, and increased the overall mortality due to HSV-1 strain F injected either i.p. or s.c. Comparable results were obtained with strain B-12. Twenty-five mice that had survived HSV inoculation (s.c. or i.p.) were injected with antiinterferon globulin 18 days after viral inoculation. In no instance did this treatment induce signs of HSV disease.

Animals↗
PubMed1977

Inhibition by anti-interferon serum of lymphocytic choriomeningitis virus disease in suckling mice.

Inoculation of newborn mice with lymphocytic chloriomeningitis (LCM) virus resulted in decreased weight gain, liver cell necrosis, and death. Injection of potent sheep immunoglobulin against mouse interferon markedly inhibited these manifestations of LCM virus disease despite the fact that these treated mice had 100-fold more LCM virus in their serum. We conclude that interferon induced by LCM virus is responsible in large part for the syndrome of growth inhibition, liver cell necrosis, and death observed in LCM virus-infected suckling mice.

Animals↗
PubMed1977

Antiviral activity of bovine interferons on primate cells.

Potent preparations of bovine leucocyte and fibroblast interferons had substantial antiviral activity on monkey cells and low activity on human cells. Thus, interferon from a 'lower' phylogenetic species can have considerable antiviral activity in primate cells, but not all primate cells are equally sensitive.

Animals↗
PubMed1977

On the mechanisms of the antitumor effects of interferon.

The effect of interferon in animals infected with some oncogenic viruses can be attributed to inhibition of viral replication or inhibition of the early events following viral infection. In those experimental systems in which continued administration of interferon proved effective after inoculation of oncogenic viruses, the effect may be due in part to an antiviral effect and in part to a direct action of interferon on the multiplication of precursor cells or tumor cells themselves. In animals bearing autochthonous tumors or grafted with transplantable tumors, the effects appear to be due in part to a a direct inhibition of the multiplication of the tumor cell (or an effect on the behavior of these tumor cells) and in part to an effect on the host - the nature of which remains to be defined. We must learn more of the interaction of interferon with host cells and understand how so many apparently different effects are triggered by this "polypractic substance" (6) before we can clarify the mechanism by which interferon can confer protection on animals infested with viruses, protozoa, or tumor cells.

Animals↗
PubMed1976

Role of interferon in the pathogenesis of virus diseases in mice as demonstrated by the use of anti-interferon serum. I. Rapid evolution of encephalomyocarditis virus infection.

The role of interferon in the pathogenesis of encephalomyocarditis (EMC) virus infection was determined by treating mice with potent, partially purified sheep anti-mouse interferon globulin. In control mice, EMC virus was present in low titers in various visceral organs but attained high titers in the brain towards the 4th to 5th day, at which time mice died with signs of central nervous system disease. In mice treated with anti-mouse interferon globulin, virus was present in high titer in visceral organs 24--36 h after viral inoculation and virtually all mice were dead by 45 h. This rapid evolution of EMC virus infection was not observed in mice treated with the globulin fraction prepared from a normal sheep, from a sheep exhibiting a low anti-mouse interferon-neutralizing titer, nor from a sheep having a high titer of antibody to human leukocyte interferon. The experimental results indicated that anti-interferon globulin neutralized the interferon liberated by virus-infected cells, thus permitting extensive virus multiplication in several visceral organs. We conclude that interferon is an important early component of host resistance to this virus infection.

Antigen-Antibody Complex↗
PubMed1976

Role of interferon in the pathogenesis of virus diseases in mice as demonstrated by the use of anti-interferon serum. II. Studies with herpes simplex, Moloney sarcoma, vesicular stomatitis, Newcastle disease, and influenza viruses.

The effect of potent sheep anti-mouse interferon globulin was investigated in several different experimental virus diseases of mice. In anti-interferon globulin-treated mice infected intraperitoneally with herpes simplex virus (HSV) type I, the latent period was shortened, and the overall LD50 was increased several hundredfold compared to virus-infected control mice. When HSV was inoculated subcutaneously all anti-interferon globulin-treated mice died, whereas only 5% of virus-infected control mice died. Subsequent treatment with anti-interferon globulin of previously HSV-infected mice did not result in reactivation of HSV. Treatment of adult mice with anti-interferon globulin resulted in an earlier appearance of MSV-induced tumors, a greater number of mice bearing tumors, an increase in tumor size, and an increase in the duration of tumors. All tumors eventually regressed despite reinjection of anti-interferon globulin. Anti-interferon globulin treatment resulted in a rapid onset of disease and death in adult mice inoculated (intranasal) with VSV and in newborn mice infected with NDV. Anti-interferon globulin exerted no effect on the course of influenza virus infection of mice. We conclude that the early production of interferon is an importane element in the response of the mouse to several viruses exhibiting different pathogeneses.

Animals↗
PubMed1976

Interferon and murine leukemia. VII. Therapeutic effect of interferon preparations after diagnosis of lymphoma in AKR mice.

Daily administration of potent mouse interferon preparations, begun after clinical diagnosis of lymphoma in AKR mice, increased average survival by approximately 100%. Interferon treatment delayed the evolution of the lymphoma but regression of tumour was not observed. The therapeutic effects observed with interferon in AKR mice compare favorably with reported results obtained using standard anti-cancer drugs.

Animals↗
PubMed1976

Relationship between the enhanced expression of histocompatibility antigens on interferon-treated L 1210 cells and their position in the cell cycle.

We have determined the cell cycle position of individual mouse leukemia L 1210 cells by cytophotometric and autoradiographic techniques and simultaneously determined the amount of histocompatibility antigens expressed on the surface of individual cells by quantitative immunofluorescence. Interferon treatment of L 1210 cells was accompanied by an enhanced expression of histocompatibility surface antigens. The distribution of interferon-treated cells in the various phases of the cell cycle was similar to that for control cells and the enhanced expression of histocompatibility antigens was observed on interferon-treated cells in all phases of the cell cycle. We conclude, therefore, that this enhancement is not due to a preferential concentration of these cells in any one particular phase of the cell cycle.

Animals↗
PubMed1976

Interferon treatment of mice: enhanced expression of histocompatibility antigens on lymphoid cells.

Treatment of young and mature mice with potent mouse interferon preparations results in a marked enhancement of the expression of histocompatibility antigens on the surface of thymocytes and splenic lymphocytes as measured by an enhanced absorption of alloantiserum. We postulate that such modifications of the cell surface may reflect an effect of interferon on lymphocyte maturation and may be relevant to the effect of interferon on lymphocyte function.

Age Factors↗
PubMed1976

Enhanced expression of histocompatibility antigens of lymphoid cells in mice treated with interferon.

Treatment of young and mature mice with potent preparations of mouse interferon results in a marked enhancement of the expression of histocompatibility antigens on the surface of thymocytes and splenic lymphocytes, as measured by an enhanced absorption of alloantiserum. These modifications in the expression of cell surface antigens may reflect an effect of interferon on lymphocyte naturation and may be relevant to theffect of interferon on lymphocyte function.

Animals↗