Search PubMed⌕ Search

Biomedical subjects

H Schellekens

Publications and source records attributed to H Schellekens.

At least 109 records · Page 6Linked to original sources
PubMed1982

Antiviral and side effects of interferons produced by recombinant DNA techniques as tested in rhesus monkeys.

Human interferon type alpha 2 (HuIFN-alpha 2) produced by Escherichia coli was found to be as active as natural leukocyte interferon in protecting rhesus monkeys against intradermal vaccinia virus infection. HuIFN-beta 1 produced in E. coli had similar but less pronounced activity. HuIFN-alpha 2 induced fever but not leukopenia, while HuIFN-beta 1 had opposite effects. Concurrent treatment with acetosalicylic acid and prednisolone/azothioprine combinations did not interfere with the efficacy of the human interferons.

Animals↗
PubMed1981

In vivo immune stimulation by interferon during viral infection.

Treatment of Rhesus monkeys with human leukocyte interferon prevents the development of skin lesions after intradermal infection with vaccinia virus. The treatment does not prevent the development of immunity to vaccinia. Inactivated vaccinia virus, which is non-immunogenic in untreated monkeys, induced immunity under interferon treatment, indicating that interferon had an immune-stimulating effect.

Adjuvants, Immunologic↗
PubMed1981

Relationship between the cellular expression of the antiviral and anticellular activities of interferon.

This study suggests that the expression of the antiviral and anticellular activities of interferon in rat cells treated with homologous interferon are closely linked. After addition and subsequent removal of interferon, the two activities appeared and disappeared simultaneously. Both activities were equally influenced by the exposure time and by the temperature during exposure to interferon. Pretreatment of the cells with cholera toxin inhibited both activities to the same extent at low interferon levels.

Animals↗
PubMed1981

Induction of natural killer cell activity and allocytotoxicity in human peripheral blood lymphocytes after mixed lymphocyte culture.

The K-562 tumour cell is a highly susceptible target for natural killer (NK) cell lysis by lymphocytes of human peripheral blood. We have studied the antigenic relationship between the recognition sites for lysis of lymphoid and various tumour target cells by cytolytic T lymphocytes (CTL) and NK cells induced in mixed lymphocyte cultures (MLC). The characteristics of these two effector cell types have also been investigated. It was demonstrated that fresh NK cells lose their NK lytic activity when cultured alone. Cell lines not susceptible to lysis by fresh NK cells are lysed by MLC-induced NK cells. There is no antigenic relationship between the recognition sites for the alloreactive T lymphocytes and MLC-generated NK cells expressed on the lymphoid target cells and the tumour target cells, respectively. The MLC-generated alloreactive T cells and NK cells are not identical. The MLC-generated NK cells are different from the fresh NK cells present in the peripheral blood.

Absorption↗
PubMed1980

Double-blind study of leucocyte interferon administration in chronic HBsAg-positive hepatitis.

In a double-blind study human leucocyte interferon was given for six weeks to 8 of 16 patients with chronic HBsAg-positive hepatitis. In the first week 12 x 10(6) reference units were administered daily, and thereafter the dose was halved every week. During the first two weeks leucopenia was observed in 6 of the 8 interferon-treated patients. Apart from a drop in DNA-polymerase activity in the first week, no effect was found on indices of hepatitis-B-virus infection.

Adult↗
PubMed1980

Influence of input multiplicity of infection on the antiviral activity of interferon.

The antiviral activity of interferon was shown to be dependent on the input m.o.i. Cells could not be protected against the cytopathogenic effect of vaccinia, herpes, Echo or vesicular stomatitis virus at m.o.i. greater than 1. At a m.o.i. of less than or equal to 1, cells could be protected but the amount of interferon necessary to yield protection was inversely related to the m.o.i. When protection was afforded, it was only transient. The duration of the antiviral effect of interferon was also inversely related to the m.o.i. The dependence of the antiviral effect on the m.o.i. could not be explained by assuming the viruses to be mixtures of subtypes with different interferon sensitivity. Also, selection by interferon treatment of interferon-insensitive subtypes could not be shown. The greater antiviral effect of interferon at low m.o.i. was probably not caused by induction of interferon by the infecting virus. A direct inactivation by the virus of the antiviral effect of interferon could not be demonstrated. These results indicate that when interferon-treated cells are infected, they will not survive the infection. The only result of the interferon treatment will be to inhibit virus replication to some extent, leading only to a delay in cell death.

Animals↗
PubMed1980

Production and initial characterization of rat interferon.

Rat interferon of relatively high specific activity (about 10(6) units/mg protein) was produced in embryonic rat cells treated with Newcastle disease virus at a high m.o.i. The cells were cultured in serum-free medium and the interferon was precipitated and concentrated with 0.02 M-zinc acetate or with ammonium sulphate at 85% saturation. With both methods the increase in interferon activity was greater than the concentration factor. The rat interferon activity was stable on treatment with 0.15 M-perchloric acid or three cycles of freezing and thawing, but incubation at 37 degrees C for 1 h resulted in a 50% loss in activity. It had no cross activity in human or mouse cells. The sensitivity of different types of rat cells for rat interferon differed widely and was dependent on the challenge virus. Human interferons had no detectable antiviral activity on rat cells and did not block the activity of rat interferon.

Animals↗
PubMed1980

Prevention of vaccinia lesions in Rhesus monkeys by human leucocyte and fibroblast interferon.

The prophylactic antiviral activity of systemically administered human interferon preparations was tested in 36 rhesus monkeys against vaccinia virus injected into the skin. All nine control monkeys developed typical vaccinia skin lesions. Eight of nine monkeys treated with daily intramuscular injections of leucocyte interferon (5 x 10(5) units/kg) from day -1 to day +7 after vaccination were completely protected. No lesions developed after discontinuation of therapy. Administration of the same amounts of leucocytic interferon intravenously (i.v.) was equally effective. Daily intramuscular (i.m.) injections of lower doses of leucocyte interferon (1.25 c 10(5) units/kg; 0.5 x 10(5) units/kg) decreased the severity of the skin lesions. Lesion scores correlated inversely with the dose of interferon. Four of six animals receiving daily i.m. injections of fibroblast interferon (5 x 10(5) units/kg) and one of three animals treated i.v. with the same dose were protected against vaccinia virus, and the lesions in the other monkeys were smaller. Intramuscular injections of 5 x 10(5) units/kg of fibroblast interferon or 1.25 x 10(5) units/kg of leucocyte interferon resulted in comparable serum levels and had comparable efficacy in reducing lesion scores.

Animals↗
PubMed1979

Differential effects of fibroblast and leucocyte interferon in HBsAg positive chronic active hepatitis.

Six patients with hepatitis B surface antigen, hepatitis B 'e' antigen positive chronic active hepatitis, and elevated hepatitis B specific DNA polymerase activity were treated sequentially with fibroblast and leucocyte interferon. Fibroblast interferon induced a fall in serum transaminase activities in all patients, whereas a consistent decline in DNA polymerase activity was observed during leucocyte interferon administration only. After treatment one patient remained persistently DNA polymerase and hepatitis B 'e' antigen negative, whereas relapse to initial values occurred in others. Side effects included severe but reversible granulocytopenia, and chills responding to promethazine treatment. The differential biologies with their non-identity in in vitro studies.

Chronic Disease↗
PubMed1979

Prophylaxis and therapy of HBsAg positive hepatitis.

Different forms of prophylaxis and therapy of HBsAg positive hepatitis are discussed. Prevention of HBsAg positive hepatitis has been attempted by passive and active immunisation. For passive immunisation against parenteral infections hepatitis B immunoglobulin (HBIG) of high titer has to be used. However, the protection provided by HBIG is incomplete and temporary. Therefore active immunisation is to be preferred for protection of high risk groups. Experiments using the 22 nm spheric particles prepared from plasma of chronic carriers showed the efficacy of this type of vaccine. The direct way to treat the different forms of hepatitis B is the eradication of the virus from the body. Success has been claimed with the use of interferon and adenine arabinoside. However, this antiviral therapy is still in an experimental stage. In some forms of HBsAg positive hepatitis the liver damage is supposed to be the result of an immune response against the virus. Immunosuppression in these conditions failed, however, to show a beneficial effect. Corticosteroids turned out to be harmful in all forms of acute hepatitis and are therefore contraindicated. Chronic hepatitis B seems to be caused by the inability of the immune system to clear the virus. Successful results have been claimed employing immune stimulative agents like BCG, levamisole, and transfer factor. Most of these reports, however, are anecdotycal and the more comprehensive studies are uncontrolled.

Adjuvants, Immunologic↗