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At least 595 records · Page 33Linked to original sources
PubMed2000

Combination of ribavirin and interferon-alfa surpasses high doses of interferon-alfa alone in patients with genotype-1b-related chronic hepatitis C.

The purpose of this study was to compare interferon-alfa alone (12-month course with high initial doses) with a combination of interferon-alfa and ribavirin in patients infected with genotype 1b. Three hundred and seven patients were randomized into 3 groups to receive 6 mega units (MU) of interferon-alfa-2b subcutaneously 3 times weekly for 6 months followed by 3 MU for 6 months (n = 95, group A); 10 MU for 3 months followed by 6 MU for 3 months, followed by 3 MU for 6 months (n = 83, group B); or the group-A schedule in combination with ribavirin (n = 129, group C) for 4 (n = 46), 6 (n = 44), or 12 months (n = 39). Negative polymerase chain reaction (PCR) was more frequent in group C than in groups A or B after 3 months of treatment (P <.006), at the end of treatment (P =.017), and at the end of follow-up (32.8%, 16.9%, and 14.1%, respectively, P <.003). A complete response (negative PCR and normal alanine transaminase) was higher in group C than in the other groups and when comparing 12- to 4- and 6-month combination therapy at the end of treatment (P =.05) and of follow-up (45.2% vs. 25.4%, respectively, P =.05). The greater efficacy of the combination was related to the higher rate of primary virological response and also to a decrease in the percentage of breakthrough and of relapse. In 1b-infected patients, the combination of high doses of interferon-alfa (6 MU) and ribavirin for 12 months appears to be the best therapy, with a high rate of sustained response.

Adult↗
PubMed1974

The somatic cell genetics of human interferon: assignment of human interferon loci to chromosomes 2 and 5.

A total of 40 mouse-human cell hybrids were induced with poly(I).poly(C) and with Newcastle disease virus. Ten hybrid clones produced low levels of human interferon in response to both the virus and poly(I).poly(C). Concurrent enzymic and chromosomal analysis of the hybrid clones indicated a concordant segregation of these levels of human interferon with chromosomes 2 and 5. The presence of both chromosomes 2 and 5 was necessary for interferon production; neither was sufficient alone. Based on this finding, we postulate that there are at least two asyntenic gene loci for the expression of interferon in human cells.

Animals↗
PubMed1981

Specific activity of pure human interferons and a non-biological method for estimating the purity of highly purified interferon preparations.

Methods for determining the specific activity and percentage purity of highly purified interferon preparations are unreliable, mainly because of the difficulty in estimating very small quantities of protein. Human leukocyte-derived interferon (HuIFN-alpha) is a mixture of several distinct species, and the relationship between specific activity and purity is not direct. A non-biological method is described here, by which the purity of highly purified HuIFN-alpha is determined chromatographically. Samples are run on a Sephadex G-75 column with continuous measurement of E206 in the eluate, and SDS gel electrophoresis is used to separate essentially all the protein species in the characteristic double peak region containing interferon activity and show that they are interferons. The validity of the method has been checked using a range of standard proteins. The specific activity of pure Namalwa (lymphoblastoid) HuIFN-alpha was estimated to be 1.0--1.7 x 10(8) U/mg protein.

Cells, Cultured↗
PubMed1984

Inhibition of anticellular activity of mouse gamma interferon by an inhibitor of interferon action.

An inhibitor of interferon's (IFN) antiviral action was evaluated for its ability to block interferon's anticellular action. Crude and partially purified mouse immune interferon (MuIFN-gamma) preparations with high and low levels of an inhibitor of IFN's antiviral action were prepared. These preparations were examined for their relative antiviral and direct anticellular activities. The inhibitor present in the IFN-gamma preparations was found to be an equally potent inhibitor of both the antiviral and the direct anticellular activities of IFN-gamma. Further, while the inhibitor of IFN-gamma was inherently present in most IFN-gamma preparations, it was not an inherent feature of all IFN-gamma molecules. Inhibitor-free IFN-gamma could be separated from inhibitor-containing IFN-gamma by column chromatography. The results suggest that the inhibitor generally antagonizes interferon action and should be taken into account when evaluating the biological properties of IFN-gamma preparations.

Animals↗
PubMed1985

The interferon compartment of the immune response in human malaria: I. Interferon inducers in Plasmodium falciparum cultures.

The present study concerns the interferon (IFN) compartment of the immune response in human malaria. It was undertaken with Plasmodium falciparum parasitized human red blood cell culture supernatants (PF-RBCS). Investigations were conducted in order to verify whether supernatants of such protozoa cultures had the capacity to induce gamma interferon previously identified in sera of P. falciparum infected patients and to verify whether a T-cell mitogen recently characterized in vitro could be correlated with the eventual IFN-inducing activity. Investigations were performed with nonsynchronized P. falciparum cultures and highly synchronized PF-RBC cycles. Results obtained with the first type of experiment demonstrated the presence of an immune interferon inductor in PF-RBCS controlled for their positive mitogenic activity. In supernatants from highly synchronized PF-RBC cycles it was possible to further correlate the mitogen activity with the capacity to induce IFN-gamma. Both activities were found in the time-interval situated near the end of the parasite cycle shortly previous of the merozoite stage. At an earlier time, at the peak of the ring stage, when no mitogen activity was detected, an interferon-induction activity, solely of IFN-alpha, was also demonstrated.

Cells, Cultured↗
PubMed1976

Influence of interferon on the synthesis of virus particles in oncornavirus carrier cell lines. IV. Relevance to the potential application of interferon in natural infectious diseases.

That interferon reduced the release of C-type oncornavirus particles by chronically infected mouse cells was shown by radiolabeling of the particles with uridine or amino acids and by determination of particle-associated reverse transcriptase. The number of released particles, as determined by direct electron microscopic enumeration, was reduced to a lesser extent. In contrast, interferon failed to affect the number of budding particles and caused a slight increase in the number of completed particles present in the microspace contiguous to the cell membranes. A working hypothesis is that, in the presence of interferon, C-type particle assembly and release are slowed but not arrested; sizable numbers of particles continue to be assembled and released. Some of these particles may be defective in one or more proteins, such as reverse transcriptase or proteins necessary for final release. These in vitro data justify speculation that, in vivo, interferon may be expected to reduce tissue damage due to antigen-antibody complex formation, but not damage due to sytolytic immune attack on cells carrying the antigens.

Animals↗
PubMed1977

Is interferon tissue specific?- Effect of human leukocyte and fibroblast interferons on the growth of lymphoblastoid and osteosarcoma cell lines.

The growth inhibitory effect of human leukocyte and fibroblast interferons was tested in vitro. The effect of fibroblast interferon was more pronounced on osteosarcoma cells and the effect of leukocyte interferon was more pronounced on lymphoid cells. This suggests that the capacity of interferon to inhibit cell growth is, in some measure, tissue specific.

Burkitt Lymphoma↗
PubMed1984

Distribution of rabies virus, interferon and interferon-mediated enzymes in the brains of virus-infected rats.

The distribution of rabies virus, interferon and interferon-mediated enzymes, pppA(2'p5'A)n synthetase (2-5A synthetase) and poly(rI) . poly(rC)-Sepharose-bound protein kinase, was studied in different regions of the brains of rabies virus-infected rats. A broad range of virus infectivity was found in the brain stem, cerebellum, cortex, hippocampus and striatum. Similarly, the levels of interferon were variable (2500 to 60 000 units/mg protein in tissue extracts) in the different brain regions studied but were unrelated to the corresponding infectivities . The level of 2-5A synthetase and protein kinase was enhanced several-fold in the individual brain regions and the degree of such enhancement was correlated with the level of interferon.

2',5'-Oligoadenylate Synthetase↗
PubMed1985

Interferon induction by viruses. XII. Inhibition of protein synthesis renders aged chick embryo cells refractory to interferon induction.

The initial stages of interferon induction in mouse L cells do not require protein synthesis; all steps in the induction process up to and including the transcription of interferon mRNA occurred in the presence of inhibitors of protein synthesis. In contrast, interferon induction in primary chick embryo cells aged in vitro does require a reaction that depends upon protein synthesis, unique in that it is not required for virus replication or the action of interferon.

Animals↗
PubMed1979

Interferon and cytotoxic factor (cytotoxin) released in the blood of mice infected with Mycobacterium bovis BCG. II. Influence of time after BCG inoculation on production of interferon and cytotoxin by capsular polysaccharide of Klebsiella pneumoniae or by bacterial lipopolysaccharide and on hyperreactivity to their lethal effects.

The time course of the occurrence of hyperreactivity in interferon and cytotoxin responses to the active substance (neutral fraction) of the capsular polysaccharide of Klebsiella pneumoniae (neutral CPS-K) and bacterial lipopolysaccharide (LPS) and of the hyperreactivity to their lethal effects was followed after infection with BCG in SMA and ICR strains of mice. The duration of these hyperreactivities of BCG-infected mice depended on the inoculum doses of BCG. The time patterns of the hyperreactivity to the lethal effects of neutral CPS-K and LPS were similar in both strains of mice, although the maximum toxicity of LPS by the intraperitoneal route in BCG-infected mice on a weight basis was stronger than that of neutral CPS-K. Irrespective of inducer and mouse strain, the time pattern of the hyperreactivity to produce cytotoxin was similar to that of the hyperreactivity to produce interferon. The patterns for these phenomena when neutral CPS-K was used as an inducer were also similar to those when LPS was used. In ICR mice the hyperreactivity in interferon and cytotoxin responses to either neutral CPS-K or LPS decayed significantly earlier than the hyperreactivity to their lethal effects, whereas in SMA mice the occurrence of both types of hyperreactivities seemed to be associated. Therefore, it is suggested that the mechanism for the hyperreactivity in interferon and cytotoxin responses to neutral CPS-K or LPS in BCG-infected mice is not necessarily the same as that for the hyperreactivity to their lethal effects.

Animals↗
PubMed1980

Antiviral and cell multiplication inhibitory activities of mouse interferon poreparations tested on an interferon sensitive murine sarcoma cell line.

The cell multiplication inhibitory effect of SDS-treated mouse interferon separated into antiviral (AV) and cell multiplication inhibitory (CMI) fractions was compared to that of untreated similar interferon on a line of murine osteosarcoma cells. The untreated interferon poreparatin and the CMI fractions dose-dependently inhibited the multiplication of the cells as measured by cell count and incorporation of 3H-thymidine into the cultures. The AV fractions, containing comparable antiviral activites as the untreated interferon preparations, had only a minor effect on cell multiplication. The biochemical properties of the fractions studied remain unknown.

Animals↗
PubMed1966

Effect of interferon on early interferon production.

Chick embryo cells given prior treatment with interferon make new interferon earlier and in larger quantities upon stimulation with Chikungunya virus than cells not so treated. By the criterion of loss of sensitivity to actinomycin, the time needed for formation of messenger RNA for interferon was decreased in the primed cells. Thus interferon affects virus action within 1 hour after infection.

Animals↗
PubMed1982

Molecular weight of human gamma interferon is similar to that of other human interferons.

The molecular weight (as determined by molecular sieve chromatography) of human gamma interferon, formerly referred to as immune or type II interferon, is between 40,000 and 70,000. On sodium dodecyl sulfate-polyacrylamide gel electrophoresis, gamma interferon activity was recovered mainly from two regions of the gels corresponding to molecular weights of 20,000 and 25,000. The results suggest that in native form human gamma interferon may be aggregated.

Glycoproteins↗
PubMed1981

Combined protective effects on interferon and interferon induction on herpes simplex and ectromelia virus infections in mice.

Mouse interferon or the induction of mouse interferon with polyriboinosinic acid-polyribocytidylic acid significantly protected mice against herpes simplex and ectromelia viral infections. When polyriboinosinic acid-polyribocytidylic acid was administered 24 h before herpes simplex or ectromelia viral infection and mouse interferon was administered shortly before and 24 h after infection, a combined protective effect against either herpes simplex or ectromelia viral infection in mice was evident. There was a significant decrease in the mortality rate with the combined treatment as compared either with the rate in group treated with interferon or polyriboinosinic acid-polyribocytidylic acid.

Animals↗
PubMed1982

Antiviral effects of interferon on a somatic cell hybrid between two Burkitt's lymphoma cell lines of different interferon sensitivities.

A somatic cell hybrid between two human Burkitt's lymphoma cell lines, Raji and Daudi, was infected with either Epstein-Barr virus or vesicular stomatitis virus after interferon treatment. Raji cells are resistant to the antiviral effects of exogenously added interferon, whereas Daudi cells are interferon sensitive. The Raji-Daudi hybrid showed an interferon sensitivity that was intermediary to that of the parental cells against both viruses.

Burkitt Lymphoma↗
PubMed2006

Analysis of mutations within the 5' untranslated region, interferon sensitivity region, and PePHD region as a function of response to interferon therapy in hepatitis C virus-infected patients in India.

Mutations in several subgenomic regions have been implicated in influencing response to interferon therapy; however, a comprehensive picture of Indian patients was lacking. Based on the viral load and clinical factors, 10 out of 15 patients were found to be complete responders, whereas 5 patients were nonresponders. The pretreatment viral RNA load of the patients was found to be between 5.20 and 6.13 log10 IU/ml, which eventually fell to 2.77 log10 IU/ml after 24 weeks of treatment, whereas in the case of nonresponders, the average was 5.38 log10 IU/ml. In order to study the influence of the hepatitis C virus genotype on the response to interferon therapy, the 5' untranslated region sequences of the samples were analyzed, which showed that genotype 3 patients responded better than genotype 1 patients. Additionally, the mutations in the interferon sensitivity-determining region (ISDR) of the NS5A protein and the double-stranded RNA-activated protein kinase-eukaryotic initiation factor 2 alpha phosphorylation homology domain (PePHD) of the E2 envelope protein, before and after treatment, were compared with nonresponder prototype J. Although, no clear correlation was found in the case of the mutated ISDR, some significant changes in residues were observed in the PePHD region, which could be helpful in understanding the molecular basis of resistance to therapy. Interestingly, analysis of the quasispecies variations showed a change in genotype in one sample during treatment, which might have contributed to the resistance. The results suggest that the mutations in different regions of the viral genome might have a concerted effect on the response to interferon therapy.

5' Untranslated Regions↗
PubMed1989

In vivo evidence of interaction between interferon-stimulated gene factors and the interferon-stimulated response element.

Constitutive and interferon-inducible DNase hypersensitive sites in vivo are located in interferon-stimulated gene promoters near sequences that specifically bind constitutive or interferon-inducible proteins in vitro. Induced sites and proteins are transient or maintained, depending on cell type. Interferon-stimulated gene transcription is transient or maintained in parallel.

Cell Line↗
PubMed1989

Randomised controlled trial of interferon alfa (lymphoblastoid interferon) in chronic non-A non-B hepatitis.

OBJECTIVE: To determine the effect of low dose interferon alfa (human lymphoblastoid interferon) on aminotransferase activities in chronic non-A non-B hepatitis. DESIGN: Prospective randomised controlled parallel group study of active treatment versus no treatment carried out over 16 weeks and preceded by baseline measurements at weeks 8 and 4 and time zero. SETTING: HEPATOLOGY outpatient clinics in secondary referral centres. PATIENTS: Fourteen adults with histologically proved chronic hepatitis and persistently raised aminotransferase activities for six months or more. INTERVENTIONS: Seven patients randomised to receive interferon alfa 5 megaunits (MU) daily for one week, reducing to 5 MU thrice weekly for seven weeks, then 3 MU thrice weekly for eight weeks. Controls not treated. END POINT: Control of hepatic enzyme activity in chronic non-A non-B hepatitis. MEASUREMENTS AND MAIN RESULTS: Serum aspartate aminotransferase activity remained raised in controls (mean increase in study period 23.4 U/l) but fell rapidly to normal in the treated group (mean decrease 106.4 U/l). In four cases values were normal by eight weeks and in five cases by 16 weeks. Only minor side effects were recorded (fever, myalgia), which became less common as treatment progressed. CONCLUSIONS: Continuous low dose interferon alfa reduces aspartate aminotransferase activity to normal in most patients with chronic non-A non-B hepatitis and may prevent progression to cirrhosis.

Adult↗