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PubMed1982

Interferon system of human cornea cells: interferon production, characterization, and development of antiviral state.

The interferon (IFN) system of human cornea cells in culture was studied. IFN produced by these cells by infection with Newcastle disease virus (NDV) was shown, by neutralization studies with specific antisera against human alpha interferon (HuIFN-alpha) and human beta interferon (HuIFN-beta), to contain 90-95% antiviral activity characteristic of the HuIFN-beta and 5-10% that of HuIFN-alpha. The chromatographic behavior of human cornea IFN on Con A-Sepharose and zinc chelate agarose columns was identical to that of HuIFN-beta produced by human foreskin cells. The cornea cells developed marked resistance when exposed to either HuIFN-beta or human gamma interferon (HuIFN-gamma) against vesicular stomatitis virus (VSV), but to a much lesser degree against HSV-1. Both the laboratory-adapted strain and a clinical isolate of HSV-1 were found to be resistant to HuIFN-beta and HuIFN-gamma as compared with VSV. The clinical isolate of HSV-1 was, however, more sensitive to HuIFN-gamma than the laboratory-adapted strain. Furthermore, a combination of HuIFN-beta and HuIFN-gamma did not significantly increase the level of antiviral state induced in cornea cells against HSV-1. These results suggest that in-vitro culture of human cornea cells can be a valuable system to evaluate the potential of chemotherapeutic agents against common ophthalmic viral infections.

Cells, Cultured↗
PubMed1984

Receptors for human alpha interferon: are gangliosides involved?

Interferon (IFN) action on cells must begin with an interaction with cellular receptors. Binding and cross-linking experiments reported earlier with purified 125I-labeled recombinant human (Hu) IFN-alpha 2 have revealed that IFN-alpha 2 binds to a specific macromolecular receptor on human cells (Joshi et al., J. Biol. Chem. 257, 13884-13887, 1982). Based on indirect evidence such as neutralization of the antiviral action of IFN preparations by gangliosides and binding of IFNs to gangliosides coupled to solid supports, it has been suggested by various investigators that gangliosides may be a part of the IFN-alpha/beta receptors. Experiments presented here indicate that gangliosides could block the antiviral activity of HuIFN-beta, but not of HuIFN-alpha, although both species of IFN bound strongly to gangliosides coupled to poly-L-lysine-agarose. Furthermore, gangliosides did not inhibit the binding of 125I-labeled HuIFN-alpha 2 to specific receptors on human cells, and this binding was competed out by unlabeled HuIFN-alpha 2 and HuIFN-alpha(LE) which were preincubated with gangliosides. However, the capacity of HuIFN-beta to compete for the receptors was abolished by preincubation with gangliosides. These results were confirmed by cross-linking experiments to identify the IFN-receptor complex by gel electrophoresis. The results indicate that at least in the case of HuIFN-alpha species, the ganglioside binding is apparently not at the active site of the IFN molecules required for interaction with the receptors on the cell surface.

Binding Sites↗
PubMed1984

Purified recombinant human leukocyte interferons IFLrA and IFLrD induce human lupus inclusions in Raji and Daudi cells.

Raji and Daudi are human B lymphoblastoid cell lines that readily form lupus inclusions (LIs; TRS) when grown in medium supplemented with leukocyte-, or fibroblast-derived interferon (IFN-alpha, -beta, respectively). WISH, MDBK, and GM2504 are three cell lines commonly used to measure antiviral activities. None of them form LIs in their antiviral response to alpha or immune (gamma)IFN. This distinguishes between the abilities of a cell to develop an antiviral state and to form LIs in response to IFN. Human (Hu) lymphoblastoid IFN and the two pure and homogeneous recombinant human IFN-alpha proteins IFLrA and IFLrD induce LIs in Raji cells and Daudi cells. In Daudi, a simultaneous inhibition of cell growth occurs. When compared by antiviral activities, IFLrA inhibits the growth of Daudi cells more, while IFLrD induces the greater frequency of LIs. According to molecular concentration, IFLrA and IFLrD at 133 X 10(-13) M induce LIs in Daudi cells to their maximum frequency. Growth inhibition for these same cell samples is also at maximum for IFLrA, but only 25% of maximum for IFLrD. Our results with Raji and Daudi cells provide evidence against a cause-and-effect relationship between these two biologic responses to IFN by Daudi cells. They also provide evidence for distinct, but interacting, intracellular pathways. This phenomenon is a new explanation for some of the biologic diversity shown for the HuIFNs-alpha.

B-Lymphocytes↗
PubMed1984

Antiviral and antiproliferative effects of interferons delivered via monoclonal antibodies.

We present in vitro experiments demonstrating the feasibility of specifically targeting IFNs by coupling to monoclonal antibodies (MAbs). Human interferon alpha (HuIFN-alpha), both natural and recombinant, were coupled to Epstein-Barr virus (EBV) membrane antigen (MA) specific MAbs and shown to retain full antiviral and antiproliferative activities when tested on several human cell lines. A series of in vitro pulsing experiments demonstrated that a minimum amount of MAb-delivered IFN exerts pronounced antiviral and antiproliferative effects on human QIMR-WIL target cells which carry EBV (viral) membrane antigens (EBV-MA+) and not on U-266 or Hep2 cell lines (EBV-MA-). Additionally the antiproliferative action of MAb-coupled rIFN-alpha appeared to be enhanced compared with that of uncoupled.

Antibodies, Monoclonal↗
PubMed1985

An inhibitor of interferon action: II. Biological properties of the IFN-gamma-associated inhibitor of interferon action.

Previously an inhibitor of interferon action had been isolated from mitogen stimulated mouse spleen cells. This inhibitor was associated with the IFN-gamma molecule and might possibly represent an altered IFN-gamma molecule which can no longer induce an effective antiviral state. This report further investigates the biological properties of this inhibitor. Inhibitor activity is independent of the virus used in the interferon assay. Inhibitor activity has also been found to be species specific. Mouse inhibitor does not inhibit the antiviral activity of either human IFN-gamma or human IFN-beta. However, inhibitor production is not limited to the mouse system. Inhibitor is also present in preparations of human IFN-gamma. The inhibitor does not appear to directly compete with IFN-gamma for a specific cell surface receptor since inhibitor activity is independent of interferon concentration. The presence of inhibitor allows a unique, albeit reduced level of antiviral protection to develop. Increasing concentrations of interferon do not increase the level of antiviral protection allowed by the inhibitor. This inhibitor of interferon action may represent a natural mechanism whereby IFN-gamma-induced effects are regulated in vivo.

Animals↗
PubMed1985

Cell to cell transmission of the "priming" effect on the induction of human fibroblast interferon.

Human fibroblast cells remain primed for IFN-beta 1 synthesis for at least 18 days after the removal of IFN-beta 1, to the same extent as cells primed shortly before induction. The maximal effect of priming is observed in cells that are treated with IFN at low cell density and are subsequently allowed to undergo several divisions. This observation suggests that the information for priming is propagated from cell to cell upon cell division. A diminished priming effect is observed after cells undergo more than three divisions in culture, suggesting a dilution of the mediator responsible for the transmission of the effect. It was not possible to demonstrate intercellular communication of the priming effect by a mediator found in the medium or by cell to cell contact. Observation that priming persists in cells for 18 days in the absence of detectable levels of IFN in the medium, but virus-resistance declines after three days supports the previous suggestion for different mechanisms involved in these two IFN-induced phenomena.

Cell Communication↗
PubMed1985

Antiviral effect of bacterially produced human interferon (Hu-IFN alpha 2) against experimental vaccinia infection in calves.

The heterologous antiviral efficiency of bacterially produced human interferon (Hu-IFN alpha 2) in the bovine species was studied, using vaccinia infection as experimental model. In a double blind experiment, young calves were intramuscularly injected daily for seven consecutive days with different doses of Hu-IFN alpha 2 or placebo, the treatment starting 24 h before intradermal inoculation of vaccinia virus. A clear protection by interferon was observed in all the IFN treated animals, although individual variations in the sensitivity to IFN were recorded. The efficiency of treatment varied according to the dose of IFN used: With the highest dose (10(6) IU/kg), complete protection could be obtained. The only side-effect observed was hyperthermia. Circulating antiviral activity appeared quite early after each IFN injection, presented a more or less biphasic kinetics, and was completely cleared after 24 h, justifying the daily treatment schedule. The first evidence of an in vivo antiviral effect of human interferon in the bovine species opens broad perspectives for a future use of interferon in veterinary medicine.

Animals↗
PubMed1986

In vitro biological activities of Escherichia coli-derived bovine interferons-alpha, -beta, and -gamma.

The infectious yields of several bovine viruses were inhibited in bovine cells treated with purified preparations of E. coli-derived bovine interferons (BoIFNs)-alpha, -beta, and -gamma. BoIFN-beta 2, encoded by one member of the BoIFN-multigene family, had more potent antiviral and antiproliferative activities than the product of one member of the class-I IFN-alpha gene family (BoIFN-alpha I1). BoIFN-beta 2 also completed more effectively than BoIFN-alpha I1 with HuIFN-alpha I2 for cell-surface receptors on bovine cells. Despite these differences, the kinetics of maximal antiviral activity were similar for BoIFN-alpha I1, BoIFN-beta 2, and HuIFN-alpha I2. In comparison to BoIFN-alpha I1 and BoIFN-beta 2, BoIFN-gamma had the least in vitro antiviral activity and required the longest contact with cells to achieve maximal protection against virus infection, but had a dramatically greater antiproliferative activity.

Animals↗
PubMed1986

A sensitive radioimmunoassay for detection of antibodies to recombinant human interferon-alpha A.

A radioimmunoassay (RIA) for the detection of antibodies to recombinant human leukocyte interferon A (rHuIFN-alpha A) in human serum has been developed and validated against the standard antiviral neutralization bioassay (ANB). The assay measures the binding of 125I-labeled rHuIFN-alpha A to immunoglobulins in serum. Aliquots of patients' sera are incubated with 125I-rHuIFN-alpha A and the complexes formed between antibodies in the sera and the 125I-rHuIFN-alpha A are precipitated with goat anti-human IgG serum. The radioactivity in the immune precipitate is a measure of the quantity of antibody (if present) in the serum. The sensitivity of this RIA is 5 ng of IgG/ml of serum.

Antibodies↗