The Production of Human Leukocyte Interferon in a Serum-Free Medium

Goore, Moshe Y.; Dickson, Judith H.; Lipkin, Saul; DiCuollo, Constantino J.

doi:10.3181/00379727-142-36954

Cited by 4 publications

(2 citation statements)

References 5 publications

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“…In the past few years great efforts have been made to produce larger amounts of human interferon. Several groups of investigators were able to induce human interferon in considerable concentration in human fibroblast cultures (2,13,23) and leukocyte cultures (9,20,24) either by synthetic or by viral inducers. Using appropriate concentration and purification procedures, for example, ultrafiltration and Sephadex gel chromatography (20), it is possible to prepare human leukocyte interferon (HIF), the activitv of which might be sufficient to produce demonstrable antiviral effects in man.…”

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confidence: 99%

Effect of human leukocyte interferon on vaccinia-and herpes virus-infected cell cultures and monkey corneas

Neumann‐Haefelin¹,

Sundmacher²,

Sauter³

et al. 1975

Infect Immun

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Pretreatment of human fibroblast cultures with human leukocyte interferon (HIF, 1,000 IU/ml) resulted in a 24-h delay of virus replication after infection with vaccinia virus and herpes simplex virus type 1 and type 2. Additional HIF treatment 24 h after infection effectively lowered the maximum yield of viral infectivity. Equal results were obtained in simian cells with 3,000 IU of HIF per ml. The spread of two cell-bound herpesviruses, varicella zoster virus and Medical Lake macaque herpesvirus, was inhibited by 2,000 IU of HIF per ml in human fibroblasts and Vero cells, respectively. Varicella zoster virus infectivity was notably reduced by HIF, whereas the latter system showed a low sensitivity. To study the effect of HIF in the infected cornea, keratitis was induced experimentally in both eyes of 12 rhesus monkeys and 12 African green monkeys by inoculation with vaccinia virus and herpes simplex virus, respectively. In each monkey one eye served as a control for the full cycle of disease. In the other eye HIF treatment was initiated prophylactically 15 h before or simultaneously with the challenge virus infection or 6 to 20 h postinfectionally or therapeutically after onset of the disease, and the treatment was continued for 2 to 7 days. Prophylactic and simultaneous administration equally resulted in inhibition of both vaccinia and herpes keratitis. Postinfectional and therapeutic administration of interferon moderated the course of keratitis slightly and shortened the period of virus shedding.

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mentioning

confidence: 99%

Effect of human leukocyte interferon on vaccinia-and herpes virus-infected cell cultures and monkey corneas

Neumann‐Haefelin¹,

Sundmacher²,

Sauter³

et al. 1975

Infect Immun

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“…The priming effect of interferon on subsequent inter-feron induction by poly(rI) poly(rC) has been established in different cell cultures (mouse L cells, rabbit kidney cells, and human diploid cells); the priming effect was generally greater if suboptimal doses of poly(rI) poly(rC) were used for eliciting the interferon response. Recently, interferon priming has been proven a successful method for scaling up the production of human interferon in either human diploid cell cultures (3,19) or leukocyte suspensions (18,34).…”

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confidence: 99%

Studies on the Mechanism of the Priming Effect of Interferon on Interferon Production by Cell Cultures Exposed to Poly(rI) · Poly(rC)

1973

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Interferon induction by poly(rI) poly(rC) in primary rabbit kidney and mouse L-929 cell cultures was markedly increased if the cells were previously treated with homologous interferon. This priming effect has been established with different times of exposure of the cells to poly(rI) -poly(rC), and was most pronounced for short pulses of contact of the polynucleotide with the cells (10 s, 1 min). Treatment of the cells with pancreatic ribonuclease immediately after their exposure to poly(rI) poly(rC) brought about a relatively greater reduction of the interferon response in interferon-primed cells than it did in unprimed cell cultures. Priming of the cells with interferon did not increase cell-binding of poly(rI) poly(rC), whether this cell-binding was measured quantitatively (by radioactivity, upon exposure of the cells to radiolabeled polymer) or qualitatively (by antiviral activity, by assaying the cell extract for virus plaque reduction). Similarly, interferon priming did not alter the sensitivity of cell-associated poly(rI) poly(rC) to extraneous ribonuclease treatment. Finally, priming with interferon did not decrease the rate of degradation of cell-bound poly(rI). poly(rC) by cellular nucleases nor did it increase the anti-nuclease potency of the cells. The exact mechanism by which previous exposure of the cells to interferon enhances subsequent interferon production, induced by either synthetic polynucleotides or viruses, has not yet been resolved.

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