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Biomedical subjects

E Lvovsky

Publications and source records attributed to E Lvovsky.

11 recordsLinked to original sources
PubMed1986

Phase I combined modality clinical trial of alpha-2-interferon and radiotherapy.

Sixteen patients were enrolled in a Phase I study of the combined use of recombinant DNA alpha-2-interferon (IFN) and radiation therapy, conducted at the Georgetown University Hospital (GUH) from February 1, 1984 to September 20, 1985. Escalating IFN doses ranging from 2.0 X 10(6) IU/m2 to 5 X 10(6) IU/m2 were administered to groups of six patients per IFN dose level. Three patients at each dose level were treated on a 5-day-a-week schedule and three patients were treated on a 3-day-a-week schedule. Significant toxicity including dehydration, infection, deep vein thrombosis, and myocardial infarction was noted throughout in patients receiving IFN five times per week, with eight of nine requiring hospitalization during the treatment course. There was one treatment-related death. In the five-times-per-week group, only 22% of patients tolerated the full initially planned IFN dosage and 44% tolerated the full initially planned radiation dosage, compared to 100 and 86%, respectively, in the three-times-per-week group. A tolerance dose and schedule of 5.0 X 10(6) IU/m2 of alpha-2-interferon administered subcutaneously three-times-per-week in conjunction with standard radiotherapy has been identified for use in future combined modality trials.

Combined Modality Therapy↗
PubMed1981

Epstein-Barr virus and Herpesvirus saimiri: sensitivity to interferons and interferon inducers.

The in vitro sensitivity of oncogenic herpesviruses, Epstein-Barr virus (EBV), and Herpesvirus saimiri (HVS) to human interferon produced by normal human leukocytes (Le), lymphoblastoid cell lines (LYI), and diploid fibroblasts (Fi) was studied. Four virus strains were used: HVS S295C, the highly oncogenic HVS S396-O, the transforming B95-8 strain of EBV, and the nontransforming P3HR1 strain of EBV. All interferons were active when applied to the cells after absorption of HVS and P3HR1-EBV, although different amounts were required to achieve 50% inhibition of HVS-induced cytopathic effect or EBV-induced early antigen (EA) expression. Transformation of human umbilical cord blood lymphocytes (HCBL) by the B95-8 strain of EBV was prevented only by Le and LYI. In these experiments, the most effective inhibitor of the oncogenic herpesviruses was Le, and the least effective was Fi. The effect of polynucleotides poly(I).poly(C) and the complex of poly(I).poly(C) with poly-L-lysine and carboxymethylcellulose on HVS and EBV was also studied. Their inhibitory action was proportionate to the ability of herpesvirus-infected cells to produce interferon. Thus owl monkey kidney cells, which produce relatively high levels of interferon, required nanogram quantities of polynucleotides to become resistant to HVS. Transformation of HCBL by B95-8-EBV was also prevented by poly(I).poly(C). In Raji cells superinfected with P3HR1-EBV, polynucleotides failed to stimulate interferon, and higher EBV-induced EA expression was observed. The percentage of P3HR1 and Raji cells spontaneously expressing EBV-associated antigens remained unchanged after exposure to either interferon or polynucleotides.

Animals↗
PubMed1981

Interferon induction in primates by stabilized polyriboinosinic acid-polyribocytidylic acid: effect of component size.

Two series of interferon-inducing complexes containing polyriboinosinic and polyribocytidylic acids, poly-L-lysine, and carboxymethyl cellulose were prepared. One series contained carboxymethyl cellulose, 27,000-molecular-weight poly-L-lysine, and either 4S, 6S, or 9S polyriboinosinic and polyribocytidylic acids. The other series contained carboxymethyl cellulose, 9S polyriboinosinic and polyribocytidylic acids, and poly-L-lysine, whose molecular weights ranged from 2,000 to 27,000. The homogeneity of these double-stranded polynucleotide complexes was confirmed by single-step thermal denaturation profiles and by single peaks in sucrose gradient velocity sedimentation. The complexes have a greater resistance to hydrolysis by ribonuclease than does polyriboinosinic-polyribocytidylic acid. The resistance to ribonuclease increased with the increasing size of polynucleotide homopolymers and poly-L-lysine. In monkeys and, to a lesser extent, in mice, serum interferon levels induced by the different complexes were related to the degree of resistance of the complexes to hydrolysis by ribonuclease. In mice, 4S, 6S, and 9S complexes of polyriboinosinic-polyribocytidylic acid, poly-L-lysine, and carboxymethyl cellulose had a higher level of toxicity than did polyriboinosinic-polyribocytidylic acid as measured by 50% lethal dose. The toxicity was parallel to the ribonuclease resistance of the complexes. It was concluded that an increase in the size of the polynucleotides and the polyamino acids in these complexes leads to higher resistance to hydrolysis by ribonuclease and to greater interferon responses in mice and rhesus monkeys.

Animals↗
PubMed1978

Topical treatment of vaccinia virus infection with an interferon inducer in rabbits.

Ointment containing 1.7 mg/g of the interferon inducer poly (ICLC) (a complex of polyriboinosinic-polyribocytidylic acid and with poly-L-lysine and carboxymethylcellulose) was effective both prophylactically and therapeutically against vaccinia virus infection in rabbit skin. Poly (ICLC)-treated animals developed higher titers of local interferon and of circulating virus-neutralizing antibodies than placebo-treated animals. Serum levels of greater than 100 units of interferon/ml were found 24 hr after application of the poly (ICLC) ointment to the skin of uninfected rabbits.

Administration, Topical↗
PubMed1977

Interferon induction by radioprotective mercaptoalkylamines and derived thiophosphates.

Radioprotective thiols (five mercaptoalkylamines and four derived thiophosphates) induced interferon and resistance to virus infection. Interferon production occurred in human and mouse nonlymphoid cell cultures. One of the thiols, S,2-aminoethylisothiourea, given intraperitoneally, protected mice against two unrelated viruses--Semliki forest virus and Herpesvirus hominis type 1. Two structurally different radioprotective thiols--the disulfide cystamine and L-cysteine--were unable to induce the firus resistance state or interferon.

Animals↗
PubMed1976

Modification of chronic hepatitis-B virus infection in chimpanzees by administration of an interferon inducer.

Chimpanzees chronically infected with hepatitis-B virus showed transient changes in several markers of infection when treated with the interferon inducer polyriboinosinic-polyribocytidylic acid-poly-l-lysine carboxymethyl cellulose. Serum Dane-particle-associated D.N.A. polymerase, e antigen and hepatitis-B surface antigen, and intrahepatic hepatitis-B surface and core antigens diminished during treatment. Defective (D.N.A.-polymerase-negative) Dane particles increased in titre transiently during treatment; these may play a role in the modulation of hepatitis-B virus infection. Humoral immune responses in chronic hepatitis-B carrier chimps were unaffected. Interferon inducers (or exogenous interferon) may be useful for the treatment of chronic hepatitis-B virus infection.

Animals↗