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At least 19 recordsLinked to original sources

PubMed1999

Intravenous recombinant interferon-beta versus interferon-alpha-2b and ribavirin in combination for short-term treatment of chronic hepatitis C patients not responding to interferon-alpha. Multicenter Interferon Beta Italian Group Investigators.

BACKGROUND: Little is known about the therapeutic role of intravenous interferon-beta in chronic hepatitis C patients unresponsive to a previous treatment with interferon-alpha. METHODS: Two hundred interferon-alpha non-responders were randomized to receive either intravenous recombinant interferon-beta or interferon-alpha-2b and ribavirin for 12 weeks. The responders in both groups were followed up for a further 48 weeks. RESULTS: At week 12 a biochemical and virologic response was documented in 42% of the patients treated with interferon-beta and in 22% of the patients treated with combination therapy. A sustained response was observed in 21% of the patients treated with interferon-beta and in 13% of those treated with combination therapy, with similar differences on intention-to-treat analysis. CONCLUSIONS: Short-term treatment with intravenous interferon-beta seems to offer a chance for sustained response in a subset of interferon-alpha non-responders. The role of long-term therapy in these patients still remains to be explored.

Adult↗

PubMed1983

Results of space experiment program "Interferon". I. Production of interferon in vitro by human lymphocytes aboard space laboratory Solyut-6 ("Interferon I") and influence of space flight on lymphocyte functions of cosmonauts ("Interferon III").

The results of the biological space experiment "Interferon" performed by two international cosmonaut crews aboard the space laboratory Solyut-6 are reported. Human lymphocytes separated from the blood of healthy donors and placed into "Interferon I" equipment could be kept for 7 days in suspension culture under spaceflight conditions. Interferon production could be induced in human lymphocytes by preparations of different origin, such as virus, synthetic polyribonucleotides, bacterial protein and plant pigment. An increased lymphocyte interferon production was observed in the space laboratory as compared to the ground control. A decrease of induced interferon production and natural killer cell activity was observed in the cosmonauts' lymphocytes on the 1st day on Earth after 7 days spaceflight.

Cell Membrane Permeability↗

PubMed1983

Results of space experiment program "Interferon". II. Influence of spaceflight conditions on the activity of interferon preparations and interferon inducers ("Interferon II").

The influence of spaceflight conditions on the biological activity of HuIFN-alpha preparations (lyophilized, in solution and in ointment) and interferon inducers was studied. In antiviral activity no difference was observed between the samples kept aboard the spaceship and the controls kept under ground conditions. The interferon inducers poly I:C, poly G:C and gossipol placed in the space laboratory for 7 days maintained their interferon-inducing capacity. The circulating interferon level in mice was the same irrespective of the induction being performed with flight or ground-control samples of inducers.

Animals↗

PubMed1989

The synergistic effect of human recombinant interferon-alpha 2a in combination with interferon-gamma and the induction of interferon-alpha 2a receptor by interferon-gamma.

An in vitro examination was made of the synergistic antiproliferative effect of recombinant interferon-gamma (IFN-gamma) with interferon-alpha 2a (IFN-alpha 2a) on human tumor cell lines, including lung small cell carcinoma QG-90, amelanotic melanoma HMV-1, renal carcinoma ACHN and Burkitt lymphoma Daudi. Sixty-four percent of HMV-1 cells and 75% of ACHN cells seeded were killed by treatment with 10 pM and 1000 pM of IFN-gamma, respectively. Furthermore, 69% of HMV-1 cells and 59% of ACHN cells were killed by 1000 pM of IFN-alpha 2a. When HMV-1 was treated first with 10 pM of IFN-gamma, and then with 1000 pM of IFN-alpha 2a, 81% of cells seeded were killed (p less than 0.001). Similarly, 89% of ACHN cells were killed by the same sequential treatment with 1000 pM IFN-gamma, and then of IFN-alpha 2a (p less than 0.001). However, adverse sequence of treatment could not produce such a synergistic result. On the surface of these susceptible cells, HMV-1 and ACHN, to both IFNs, the number of receptors for IFN-alpha 2a increased significantly after treatment with IFN-gamma without any serious change of the dissociation constant, suggesting that increase in the number of receptors for IFN-alpha 2a may be the major mechanism of the synergistic effects of IFN-gamma with IFN-alpha 2a.

Cell Division↗

PubMed2002

Ribavirin with or without alpha interferon versus no intervention, placebo or alpha interferon for chronic hepatitis C.

BACKGROUND: Hepatitis C is a major cause of liver-related morbidity and mortality. Ribavirin plus interferon combination therapy is presently considered the optimal treatment of interferon naive patients with chronic hepatitis C, but its role in relapsers and non-responders to previous interferon therapy is not established. OBJECTIVES: To assess the efficacy and safety of ribavirin alone or in combination with alpha interferon in interferon naive patients, relapsers, and non-responders with chronic hepatitis C. SEARCH STRATEGY: Eligible trials were identified through electronic databases, manual searches of bibliographies and journals, authors of trials, and pharmaceutical companies producing ribavirin or interferon (August 2001). SELECTION CRITERIA: We included all randomised trials comparing ribavirin with or without alpha interferon versus no intervention, placebo, or alpha interferon for chronic hepatitis C. DATA COLLECTION AND ANALYSIS: The primary outcome measures were the 'sustained' (six months after treatment) virological response, and morbidity plus mortality. The secondary outcome measures were the 'end of treatment' and 'sustained' biochemical response, the 'end of treatment' virologic response, histology, quality of life, and adverse events. MAIN RESULTS: We included eight trials in which 271 patients were randomised to ribavirin versus placebo or no intervention and 48 trials in which 6585 patients were randomised to interferon with or without ribavirin. Compared with placebo or no intervention, ribavirin monotherapy had no significant effect on the virological response or histology and only a transient effect on the biochemical response. Compared with interferon, combination therapy reduced the risk of not having a sustained virological response by 26% in naive patients (relative risk (RR) 0.74; 95% confidence interval (CI) 0.70-0.78), 33% in relapsers (RR 0.67; 95% CI 0.57-0.78), and 11% in non-responders (RR 0.89; 95% CI 0.83-0.96). There was no significant effect on morbidity plus mortality (Peto odds ratio 0.45; 95% CI 0.19-1.06). Irrespective of previous therapy, combination therapy significantly reduced the risk of not having a sustained biochemical response (RR 0.76; 95% CI 0.59-0.84) or improved histology (RR 0.67; 95% CI 0.56-0.81). Combination therapy also significantly increased the risk of treatment discontinuation (RR 1.28; 95% CI 1.07-1.52) and several types of adverse events. REVIEWER'S CONCLUSIONS: Combination therapy increased the number of naive patients, relapsers, and non-responders with a sustained virological, biochemical, or histological response, but also the occurrence of adverse events.

Antiviral Agents↗

PubMed1990

Interferons and bone. A comparison of the effects of interferon-alpha and interferon-gamma in cultures of human bone-derived cells and an osteosarcoma cell line.

Recombinant human interferon-alpha 2C and recombinant human interferon-gamma (5-1000 U/ml) inhibit the proliferation of normal human bone-derived cells and a human osteosarcoma cell line. In the bone-derived cells the inhibitory effect of interferon-gamma was significantly greater than that of interferon-alpha, whereas in the osteosarcoma cell line the inhibitory effects of both interferons were quantitatively similar. Interferon-alpha did not affect the alkaline phosphatase activity of either type of cells. In contrast, interferon-gamma affected the activity of the enzyme in both cell types: in the bone-derived cells the effect of interferon-gamma was stimulatory whereas in the osteosarcoma cells the effect was inhibitory. In both cell types interferon-gamma selectively inhibited the incorporation of radiolabelled proline into type I collagen. In the osteosarcoma cells, the effects of both interferons on collagen synthesis were quantitatively similar. In the bone-derived cells, however, interferon-alpha decreased proline incorporation into collagen and non-collagen proteins to a similar extent and thus did not affect collagen synthesis when expressed as a percentage of total protein synthesis. Two-dimensional polyacrylamide gel electrophoresis of the radiolabelled proteins of the cell layer synthesised by both cell types in the presence of either interferon demonstrated that this treatment enhanced or induced the synthesis of a total of 21 individual proteins (19 in bone cells, 14 in osteosarcoma), ranging in apparent molecular mass over 14-87 kDa. The set of proteins induced was different in all four combinations of cells and interferon. A tentative identification of several of the proteins was possible based upon estimation of molecular mass, preferential induction by interferon-alpha or interferon-gamma and differential induction in normal and transformed bone-derived cells. The results of this study demonstrate that interferons have complex effects upon the proliferative and biosynthetic activities of human bone-derived cells and demonstrate significant differences between the responses of normal cells and transformed bone-derived cell line. Further investigations will be required in order to determine whether or not these differences are unique to the osteosarcoma cell line or are a characteristic of the effects of interferons on bone-derived cells in general.

Adolescent↗

PubMed1984

Synthesis of interferon-inducible proteins is regulated differently by interferon-alpha and interferon-gamma.

Both interferon-alpha and interferon-gamma induce the synthesis of several proteins in resting human fibroblasts. Synthesis of two such proteins of Mr 67,000 and 56,000 was transient in interferon-alpha-treated cells, peaking around 6 hr after the beginning of interferon treatment and then declining to very low levels even if interferon-alpha was present continuously in the culture medium. In contrast, in cells treated with interferon-gamma, their synthesis continued unabated even 22 hr after interferon treatment began. Constant presence of interferon-gamma in the culture medium was, however, necessary for the continued synthesis of these proteins. The kinetics of their synthesis in cells treated with both interferon-alpha and interferon-gamma were similar to those in cells treated with interferon-gamma alone. Cells treated with interferon-alpha for 6 hr or with interferon-gamma for 24 hr contained in vitro-translatable mRNAs for these proteins, whereas such mRNAs were below detectable levels in untreated cells. Surprisingly, cells which had been treated with interferon-alpha for 24 hr, and which were synthesizing little of these two induced proteins in vivo, contained substantial amounts of mRNAs for these proteins, as demonstrated by in vitro translation experiments. It appears, therefore, that synthesis of some interferon-inducible proteins is regulated both transcriptionally and translationally, and the nature of such regulations is different for different types of interferons.

Cell Line↗

PubMed2001

Interferon and ribavirin vs interferon alone in the re-treatment of chronic hepatitis C previously nonresponsive to interferon: A meta-analysis of randomized trials.

CONTEXT: Hepatitis C is the leading cause of chronic liver disease in the United States. Several trials have found that interferon and ribavirin combination therapy is more efficacious than interferon monotherapy for previously untreated patients and those who relapsed after prior interferon monotherapy, but its effectiveness for nonresponders to prior interferon monotherapy is unclear. OBJECTIVE: To assess the efficacy and safety of interferon and ribavirin vs interferon alone for treatment of patients with chronic hepatitis C who previously did not respond to interferon monotherapy. DATA SOURCES: A systematic search was performed using MEDLINE and the Science Citation Index for publications from 1966 to December 1999. A manual reference search and a manual review of relevant specialty journals also were performed, and input from clinical hepatology experts was sought. STUDY SELECTION: Included studies were randomized, controlled clinical trials comparing interferon and ribavirin with interferon alone and reporting virological and biochemical outcomes after a follow-up period. Of 50 identified studies, 12 trials (941 patients) were included in the analysis. DATA EXTRACTION: Two investigators reviewed trials independently for methods, inclusion and exclusion criteria, and outcomes. Disagreements were resolved by discussion. Abstracted data included study and patient characteristics and virological, biochemical, and histological outcomes. A quality evaluation questionnaire was used to score studies. DATA SYNTHESIS: The pooled virological response rate for combination therapy was 14% (95% confidence interval [CI], 11%-17%), with a risk difference favoring combination therapy of 7% (95% CI, 2%-13%). Use of interferon alfa-2a/2b and ribavirin, 1000 to 1200 mg/d, was associated with a pooled virological response rate of 18% and a risk difference of 16% (95% CI, 11%-21%). When interferon alfa-n/n3 and a lower dosage of ribavirin (600-800 mg/d) were used, the risk difference was 0% (95% CI, -7% to 7%). Combination therapy was associated with more adverse effects and an increased rate of discontinuation of treatment compared with interferon monotherapy. CONCLUSIONS: For chronic hepatitis C that is nonresponsive to prior interferon monotherapy, combination therapy is more effective than re-treatment with interferon alone. Response rates remain less than 20% even in the most responsive subgroups, demonstrating a need for better therapeutic options.

Antiviral Agents↗

PubMed1980

Interferon in experimental viral infections in mice: tissue interferon levels resulting from the virus infection and from exogenous interferon therapy.

In mice given single intraperitoneal doses of interferon, serum interferon levels peaked at 1 h postinjection and were reduced to zero at about 8 h. The interferon concentrations in spleen, liver, and lungs were about 100-fold higher than could be expected from the amount of serum contained in these organs. In the brain only low levels of antiviral activity were detected. In mice infected intraperitoneally with Mengo virus, viral replication in the brain occurred around day 4 and was accompanied by the appearance of large amounts of interferon (approximately 10(3.25) U/g). This was preceded, however, by viral replication in the spleen and by the appearance of modest amounts of interferon in spleen and serum. In these mice protection could be obtained with relatively small doses of interferon, provided protection could be obtained with relatively small doses of interferon, provided they were given before the time of maximal levels of endogenous serum interferon. In mice infected intranasally with vesicular stomatitis virus, virus replication in the brain started within 24 to 48 h and increased with time; also, small amounts of interferon (10(2) to 10(2.5) U/g) were already detectable on days 1 and 2. The major peak of virus replication in the brain occurred on days 5 to 6 and was accompanied by the appearance of large amounts of interferon (approximately 10(3.25) U/g). In this model early treatment with interferon also provided protection, but only if given in larger doses than in the Mengo virus system. Athymic (nu/nu) mice developed a chronic systemic infection when inoculated with a demotropic strain of vaccinia virus. No interferon was detected in sera, livers, spleens, or lungs of these animals; some mice had low levels of interferon-like antiviral activity in the brain, but no attempt was made to characterize this material. Daily administration of large doses of interferon failed to exert an effect on the development of this chronic disease. Yet, normal (NMRI) mice were protected against acute infection with dermotropic or neurotropic strains of vaccinia virus, and athymic mice were partially protected against acute lethal infection with neurotropic vaccinia virus.

Animals↗

PubMed2001

Interferon-beta (INF-beta) antibodies in interferon-beta1a- and interferon-beta1b-treated multiple sclerosis patients. Prevalence, kinetics, cross-reactivity, and factors enhancing interferon-beta immunogenicity in vivo.

We analysed the role of dosage, route and frequency of administration of clinical grade interferon-beta (IFN-beta) preparations in inducing anti-IFN-beta antibodies (IFN-beta-Abs) in 5 groups of relapsing-remitting multiple sclerosis (RRMS) patients who were respectively treated as follows: 1) weekly intramuscular (i.m.) injections of 30 mg of recombinant IFN-beta1a (Avonex), 2) subcutis (s.c.) injections of 250 mg IFN-beta1b (Betaferon) every other day, 3) weekly i.m. injections of 250 mg IFN-beta1b (Betaferon), 4) s.c. injections of 22 mg of IFN-beta1a (Rebif) three times a week, and 5) i.m. injections of 22 mg of IFN-beta1a (Rebif) twice a week. IFN-beta-Abs were determined by ELISA. IFN-beta1b was more immunogenic than IFN-beta1a not only when administered s.c. every other day, but also when administered i.m. at a lower weekly dose; i.m. injection, however, significantly delayed the appearance, and induced lower serum levels of IFN-beta-Abs. In patients treated with s.c. IFN-beta1b, Ab levels peaked 3 to 9 months after therapy initiation, and then slowly, but progressively, declined to pre-therapy levels that in some patients were reached after three years. Patients treated with i.m. or s.c. IFN-beta1a only rarely developed IFN-beta-Abs, and then at very low titers. Overall, the i.m. weekly administration of IFN-beta1a was the less immunogenic treatment. In IFN-beta1b-treated patients, a wash-out period of two/three months was sufficient to bring the IFN-beta-Ab levels below the cut-off. Our findings suggest that the immunogenicity of IFN-beta1a is low, regardless of the route of administration and the dosage, while that of IFN-beta1b is high, and is significantly, but not completely reduced by i.m. administration. As IFN-beta-Abs are cross-reactive, a wash-out period is suggested when the preparation is changed from IFN-beta1b to IFN-beta1a in order to maintain the clinical benefits of the therapy.

Antibodies↗

PubMed1986

Anti-tumor effects of interferon in mice injected with interferon-sensitive and interferon-resistant friend leukemia cells. IV. Definition of optimal treatment regimens.

Mouse interferon alpha/beta exerted a similar anti-tumor effect in DBA/2 mice injected i.p. with Friend erythroleukemia cells (FLC) either sensitive or resistant to interferon as determined by both in vitro and in vivo assays. Using this tumor system we attempted to define optimal treatment regimens for interferon administration. Interferon was most effective when injected at the site of tumor inoculation rather than at a distant site. Two factors seemed of especial importance: the amount of interferon injected and the frequency of interferon administration. Thus, for daily administration of interferon, the antitumor effect was directly related to the amount of interferon injected. For a given total dose of interferon, repeated administration of small doses of interferon was more effective than administration of a larger dose at more widely spaced intervals. The anti-tumor efficacy of interferon was independent of the number of FLC inoculated when 10(2) to 10(5) FLC were injected, but interferon treatment was less effective when 10(6) or 10(7) FLC were injected. The relevance of these results to the use of interferon in patients with cancer is discussed.

Animals↗

PubMed1982

Antitumor effects of interferon in mice injected with interferon-sensitive and interferon-resistant Friend leukemia cells. I.

Interferon-sensitive (745) and interferon-resistant (3C1-8) Friend leukemia cells (FLC) are highly tumorigenic for DBA/2 mice. The phenotype of interferon sensitivity or resistance does not change with in vivo passage. Daily administration of mouse interferon markedly enhanced the survival time of mice injected with either 745 or 3C1-8 cells. Use of quantitative methods for determining the number of FLC (colony formation in agarose and immunofluorescence) permitted us to show that potent, partially purified or highly purified mouse interferon (s.a. 0.5 to 1 X 10(9) u/mg protein) induced a 100- to 1,000-fold decrease in the number of tumor cells in the peritoneal cavity in the days following inoculation of 745 or 3C1-8 cells. Interferon decreased the number of FLC even when treatment was initiated at a time when tumor cells were multiplying exponentially in the peritoneal cavity. There was no evidence that interferon acted as an inducer of FLC differentiation in vivo. The finding that interferon was equally effective in mice inoculated with interferon-resistant cells as in mice inoculated with interferon-sensitive cells suggests that in this experimental system interferon does not act directly on the tumor cells, but that the interferon-induced antitumor activity is mediated by the host.

Animals↗

PubMed1990

Induction of interferon-alpha by interferon-beta, but not of interferon-beta by interferon-alpha, in the mouse.

The antigenicity of the interferon (IFN) produced in transgenic mice carrying an extra mouse IFN-beta gene under the control of mouse metallothionein-I enhancer-promoter was examined after induction with Cd2+. Unexpectedly, IFN-alpha in addition to IFN-beta was detected in the serum. Induction of IFN-alpha was also observed when recombinant mouse IFN-beta was injected into normal mice. IFN-alpha was first detected in the circulation 6-10 hr after the administration of IFN-beta, and after 12 hr, IFN-alpha became the major component of serum IFN. On the other hand, when IFN-alpha was injected, no production of IFN-beta was observed. Messenger RNAs specific for IFN-alpha and endogenous IFN-beta were detected in the spleen, though the amount of IFN-beta mRNA was much less than that of IFN-alpha mRNA. These mRNAs were not detected in other organs including the liver where exogenous IFN-beta gene was markedly expressed. These observations showed that the expression of IFN-alpha is inducible by IFN-beta in the mouse, and the spleen was suggested to be the main site of production. Possible mechanisms of the induction are discussed.

Animals↗

PubMed2004

A randomized controlled trial of amantadine plus interferon-alpha2a vs. interferon-alpha2a alone in naive patients with chronic hepatitis C randomized according to the early virological response to interferon-alpha2a monotherapy.

BACKGROUND: An early virological response to interferon-alpha treatment is a strong predictor of sustained response, but it has never been exploited to stratify patients in clinical trials. AIM: To evaluate the efficacy of amantadine plus interferon-alpha compared with interferon-alpha alone in naive patients with chronic hepatitis C who were randomized on the basis of the early virological response to interferon-alpha. METHODS: One hundred and eighty-one patients received recombinant interferon-alpha2a (3 MU three times weekly) for 2 months and 164 were evaluated for early (i.e. month 2) virological response. Hepatitis C virus (HCV) RNA-negative patients (n = 66) were randomized to receive 3 MU of interferon-alpha three times weekly, with or without amantadine (200 mg/day); HCV RNA-positive patients (n = 98) were randomized to receive 6 MU of interferon-alpha three times weekly, with or without amantadine (200 mg/day). HCV RNA-positive patients at 6 months discontinued treatment, and all others completed 12 months. RESULTS: At month 6, HCV RNA-negative patients made up 54.2% of the interferon + amantadine group and 42.0% of the monotherapy group (P = 0.07). At month 12, HCV RNA-negative patients made up 38.5% of the interferon + amantadine group and 28.4% of the monotherapy group (N.S.). The sustained virological response rates were 21.6% and 20.9%, respectively (N.S.). CONCLUSION: The addition of amantadine does not enhance the sustained virological response to interferon-alpha in naive patients with chronic hepatitis C; however, an additive effect of amantadine occurs in the first 6 months, mainly in patients without an early response to monotherapy. Early response to interferon-alpha is a strong predictor of sustained virological response.

Adolescent↗

PubMed1990

Purification and cloning of interferon-stimulated gene factor 2 (ISGF2): ISGF2 (IRF-1) can bind to the promoters of both beta interferon- and interferon-stimulated genes but is not a primary transcriptional activator of either.

Interferon-stimulated gene factor 2 (ISGF2) was purified from HeLa cells treated with alpha interferon. The factor, a single polypeptide of 56 kilodaltons (kDa), bound both to the central 9 base pairs of the 15-base-pair interferon-stimulated response element (ISRE) that is required for transcriptional activation of interferon-stimulated genes and to the PRD-I regulatory element of the beta interferon gene. ISGF2 was a phosphoprotein, and dephosphorylation in vitro reduced its DNA-binding activity. However, conditions that changed the amount of ISGF2 did not change the phosphorylated isoforms in vivo. ISGF2 in unstimulated cells existed in trace amounts and was induced by both alpha interferon and gamma interferon as well as by virus infection. Plasmid-bearing Escherichia coli clones encoding ISGF2 were selected with antibody against purified ISGF2. Sequence analysis revealed that the ISGF2 protein was the same as that encoded by the cDNA clone IRF-1, which has been claimed to activate transcription of interferon genes. We show that transcription of the ISGF2 gene was induced by alpha interferon, gamma interferon, and double-stranded RNA. However, ISGF2 was neither necessary nor sufficient for induced transcription of the beta interferon gene, while the factor NF kappa B was clearly involved.

Base Sequence↗

PubMed2001

Interferon-alpha2a/ribaviran versus interferon-alpha2a alone for the retreatment of hepatitis C patients who relapse after a standard course of interferon.

AIM: To compare the efficacy of a descalating dose of interferon (48 weeks) versus a combination therapy of interferon and ribavirin (24 weeks) in hepatitis C positive subjects who relapsed within six months of cessation of a standard six month course of interferon three million units thrice weekly. METHODS: All 32 subjects had biopsy proven chronic hepatitis C, were PCR positive and had elevated transaminase enzymes at least one and a half times the upper limit of normal. Subjects were randomly assigned to either a descalating dose of interferon-alpha-2a; six million units thrice weekly for 24 weeks followed by 3 MIU 3x for 24 weeks or interferon three million units thrice weekly for 24 weeks plus ribavirin 1,000 mg/day for 12 weeks. A complete virological response was defined as a negative PCR for HCV RNA at 24 weeks after cessation of therapy. RESULTS: Sixteen patients were assigned to each arm and the sustained virological response was 50% for both the interferon and combination therapy arm (pNS). The biochemical response correlated with the virological response; 7/8 virological responders in the interferon alone had normalisation of transaminase 24 weeks post treatment as did 8/8 of those in the combination arm. One patient withdrew from treatment in the descalating interferon group and three required dose reduction. No subjects in the combination arm discontinued therapy but dose reduction was required in three subjects. CONCLUSION: High dose descalating interferon-alpha 2a and a combination of interferon-alpha 2a and ribavirin were effective in achieving a sustained virological response in 50% of subjects who had relapsed after a standard six month course of interferon.

Adult↗

PubMed1985

Isolation of Daudi cells with reduced sensitivity to interferon. III. Interferon-induced proteins in relation to the phenotype of interferon resistance.

The pattern of both constitutive and interferon-induced proteins was determined by two-dimensional gel electrophoresis in parental and interferon-resistant clones of Daudi cells in relation to the phenotype of interferon resistance. The complement of constitutive proteins present in clones DIF3, DIF8, DIF9 and DIF10 appeared to be identical to that of parental Daudi cells even though these cells were resistant to both the antiviral and anti-proliferative actions of interferon. Treatment of Daudi cells for 20 h with 10(3) reference units/ml of electrophoretically pure human interferon-alpha resulted in the induction of 15 proteins of molecular weights ranging from 15000 to 62000 detected after a 4 h labelling period with L-[35S]methionine. A number of these proteins were also induced in interferon-resistant clones of Daudi cells although some of these proteins appeared later and in smaller amounts than in the interferon-treated parental cells. However, seven proteins with molecular weights ranging from 18000 to 58000 which were induced by interferon in parental Daudi cells were not induced in any of the four interferon-resistant clones, suggesting that the phenotype of interferon resistance of these cells may be related to a reduction or absence of certain interferon-induced protein(s).

Cells, Cultured↗

PubMed2001

Prolonged interferon treatment after combination interferon and ribavirin therapy in patients with chronic hepatitis C: a clinical trial of interferon relapsers and non-responders.

BACKGROUND AND PURPOSE: For the retreatment of chronic hepatitis C patients relapsing after, or non-responsive to, previous interferon therapy, the efficacy of combination therapy with interferon alfa plus ribavirin is superior to interferon alone. The aim of this study was to determine whether prolonged interferon alfa treatment after 24-week combination therapy can further increase the efficacy of combination therapy. METHODS: Nineteen interferon relapsers and 17 interferon non-responders were randomly assigned to receive either interferon alfa 5 million units (MU) thrice weekly plus oral ribavirin 1,200 mg daily for 24 weeks (regimen A) or interferon alfa 5 MU thrice weekly plus oral ribavirin 1,200 mg daily for 24 weeks followed by interferon alfa 3 MU thrice weekly for another 24 weeks (regimen B). Efficacy was assessed by normalization of serum aminotransferase concentrations and disappearance of serum hepatitis C virus (HCV) RNA at the end of treatment and at 24 weeks after stopping treatment. RESULTS: Overall, 67% of relapsers receiving regimen A and 80% of those receiving regimen B had sustained virologic responses 24 weeks after stopping treatment. In contrast, 45% of non-responders receiving regimen A and 63% of those receiving regimen B had sustained responses. The sustained response was more common in relapsers with non-1b HCV genotypes. The sustained response rate to combination therapy was 50% or more in patients with genotype 1b infection. CONCLUSIONS: Prolonged interferon treatment after combination therapy has a comparable efficacy to combination therapy alone for the retreatment of chronic hepatitis C patients relapsing after, or non-responsive to, previous interferon therapy.

Adult↗