[Viferon efficacy in influenza in adult patients].

The therapeutic efficacy of Viferon (suppositories of human recombinant interferon alfa-2) was investigated in a double-blind controlled study with the use of Arbidol as a reference drug in the treatment of patients with influenza. Viferon and Arbidol lowered the signs of the fever, intoxication, catarrh and the disease as the whole.

[Viferon suppositories in the treatment of influenza in adults].

One hundred and one patients at the age of 18 to 60 years suffering from influenza were observed during increased ratio of the sickness due to the influenza virus types A (H1N1 and H3N2) and B. The diagnosis of influenza was confirmed by the laboratory tests. Viferon was used in the treatment of 35 patients. The randomized double blind placebo-controlled study revealed high therapeutic efficacy ofviferon and its immunomodulating effect on the T-cells, the neutrophil phagocytic activity and the decrease of the levels of the circulating immune complexes. Viferon and arbidol decreased the fever periods and the toxicosis symptoms vs. the placebo. The therapeutic efficacies of viferon and arbidol were on the whole comparable, whereas the clinical findings and the results of the immunological tests were evident of the viferon higher therapeutic and immunomodulating efficacy. No side effects of the drugs were recorded. The tolerability was excellent. Viferon can be recommended for the treatment of influenza in adults.

[Evaluation of the efficacy of wiferon and arbidol in adult influenza].

The therapeutic efficacy of wiferon (recombinant alpha2beta-interferon) versus arbidol was studied in a double-blind controlled study in patients with laboratorily verified influenza. Within the first 24-36 hours after the onset of the disease, wiferon and arbidol reduced the duration of fever, intoxication, and the catarrhal symptoms of the disease as a whole. The agents were shown to have an immunomodulating effect.

[Antiproliferative activity of different preparations of human interferons]. / Antiproliferativnaia aktivnost' razlichnykh preparatov chelovecheskikh interferonov.

The conclusion that the AP activity of IFN in the ChLI-1 preparation was not lost but masked by an admixture of obscure factors was drawn on the basis of coefficients of AV/AP ratio titres of IFN-alpha preparations of various degrees of purification prepared at the Gamaleia Institute of Epidemiology and Microbiology and the shape of curves of the AP effect. It was found that the curve of AP activity of diluted interferon may be of parabolic shape which reflected AP effect of high and low concentrations in the absence of AP effect for some intermediate dilutions. This is due to competitive relationships of the growth-stimulating factors and IFN upon non-simultaneous elimination of its individual subtypes. The existence of a curve of such shape indicates the expediency of testing lower concentrations than those which are characterized by a sigmoid shape of curves of AP activity, especially for cells with low sensitivity to interferon.

[Ratio of the antiproliferative action of interferon to the degree of purity of the preparation]. / Zavisimost' antiproliferativnogo deistviia interferona ot stepeni ochistki preparata.

The antiproliferative (AP) action of human leukocytic interferon (HLI) of varying degrees of purification was studied and compared in cultures of human cells differing in interferon sensitivity. The concentrated and purified preparations of HLI suppressed the incorporation of 3H-thymidine and mitotic activities of the cultures sensitive to HLI of the cells, affecting, but insignificantly, the proliferation of the resistant cell culture. Poorly purified HLI suppressed the proliferation of both cell types. This indicates that native HLI contains impurities that have an AP action and exerts no antiviral activity.

[Recovery of the sensitivity of J-41 cells to Coxsackie B3 virus by treatment with exogenous alkaline phosphatase]. / Vosstanovlenie chuvstvitel'nosti kletok J-41 virusu Koksaki B3 s pomoshch'iu obrabotki ékzogennoi shchelochnoi fosfatazoí.

It has been shown that injection of G-41 cell cultures, deficient as regards alkaline phosphatase and resistant to Coxsackie B3 virus, in conjunction with exposure to an alkaline phosphatase preparation from the calf intestine results in virus reproduction. Depending on the dose administered and multiplicity of infection there occur either complete destruction of the monolayer or death of some cells with the development of cytopathic changes specific for Coxackie virus.

[Restoration of the sensitivity of cells resistant to Coxsackie B3 virus after treatment with sensitive cell filtrate]. / Vosstanovlenie chuvstvitel'nosti kletok, rezistentnykh k virusu Koksaki B3, pri obrabotke ikh fil'tratom chuvstvitel'nykh kletok.

The study was done with J-96 cell line sensitive to Coxsackie B3 virus and the subline J-41 derived from it and resistant to this virus. In order to determine the substrates responsible for the susceptibility or resistance of these cells to Coxsackie B3 virus, homogenates and filtrates of the susceptible cells were inoculated into resistant ones and vice versa. Inoculation of the resistant cell homogenates into the susceptible cells at various intervals after virus inoculation did not inhibit virus development. Inoculation of a filtrate of the susceptible cells into resistant ones followed by long-term cultivation resulted in restoration of the susceptibility. Reversion of susceptibility to Coxsackie B3 virus was gradual and accompanied by restoration in the cells of positive Homari test to alkaline phosphatase. The positive result was obtained twice in the absence of reversion in control cells not treated with the filtrate.

[Formation of heterosymplasts in human reticular cell cultures]. / Obrazovanie geterosimplastov v kul'turakh retikuliarnykh kletok cheloveka.

The cell fusion has been studied in human reticular cell cultures J-96 and J-41 treated with the Sendai virus or with polyethylene glycol 1000 and 6000. The J-96 cells have a high alkaline phosphatase activity, in J-41 cells the enzyme is not detectable. No heterogenous alkaline phosphatase activity was seen in the protoplasm of symplasts 18 hours after virus cell fusion. It has been shown with polyethylene glycol treatment that during the fusion of cells J-96 and J-41 the enzyme activity was spreading over the symplast protoplasm.

[Cytologic and histochemical study of cell cultures chronically infected with fixed rabies virus]. / Tsitologicheskoe i gistokhimicheskoe izuchenie kletochnykh kul'tur, khronicheski infitsirovannykh fiksirovannym virusom beshenstva.

Cytoplasmic inclusion bodies corresponding in their tinctorial properties to Negri bodies were detected in TEp-2/2 and BHK-21/13S cell cultures chronically infected with fixed rabies virus. The number of cells containing the inclusions was always than that of the cells producing virus-specific antigen. Histological examinations of chronically infected cultures revealed considerable inhibition of the acid phosphatase activity, some weakening of the reaction to alkaline phosphatase, and a marked decline in the activity of succinate dehydrogenase. The intensity of reaction to RNA in chronically infected cultures was increased, particularly in those zones of the cells where RNA-containing inclusions were detected. The activity of the respiratory enzyme HAD-H2 tetrasolium reductase in HEp-2/2 cells was reduced and in BHK-21/13S cells increased as compared to the control.

[Relationship between manifestation of hyporeactivity (tolerance) in interferon production and the presence of a viral interferon inductor in the cells of the tolerant animal]. / Izuchenie sviazi mezhdu proiavleniem giporeaktivnosti (tolerantnosti) v interferonogeneze i nalichiem v kletkakh tolerantnogo zhivotnogo virusnogo induktora interferona.

Experiments revealed parallelism between the duration of the main manifestations of the hyporeactivity phenomenon (tolerance) in interferon induction and the duration of detection of a masked infection with the inducer virus (Newcastle disease virus) in peritoneal exudate cells of tolerant mice. It was also shown that after contact of chick fibroblasts with a dose of interferon which completely inhibited replication of vesicular stomatitis virus infecting the cells this virus was found in the cells in the masked form. Persistence of a virus interferon inducer in the masked form appears to play a significant role in the mechanism of tolerance as well as creation in the interferon-treated cells of conditions for masking viruses infecting these cells.

[Stimulation of the inhibiting effect of interferon on the growth of ascitic carcinoma in relation to host responsiveness and cells]. / Stimuliruiushchee ili ingibiruiushchee vliianie interferona na razvitie astsitnoi kartsinomy v zavismosti ot reaktivnosti organizma i kletok

When Krebs-2 ascitic carcinoma is transplanted to mice, administration of interferon may produce either a stimulating or an inhibiting effect on replication of carcinoma cells in the peritoneal cavity depending on the responsiveness of mice (intact or vaccinated with Newcastle disease virus) and the state of the transplanted cells ("common" or "tolerant"). Parallelism was observed in changes of the intensity of cell multiplications and indices of their enzymatic activity under the influence of exogenic interferon.

[Reasons for lowered resistance to Krebs 2 ascitic carcinoma in mice in a state of hyporeactivity (tolerance) to a viral interferon inducer]. / Prichiny snizheniia rezistentnosti k astsitnoi kartsinome Krebs-2 u myshei v sostoianii giporeaktivnosti (tolerantnosti) k virusnomu induktoru interferona

Decreased resistance to Krebs-2 ascitic carcinoma was demonstrated in mice which were in the state of hyporesponsiveness (tolerance) to virus interferon inducer (NDV) and increased resistance of the control mice to transplantation of tolerant carcinoma cells. Manifestations of tolerance in peritoneal and carcinoma cells were shown to be identical: interferon production and reproduction of vesicular stomatitis virus were inhibited, the number of viable cells was reduced, masked infection with NDV was detected, and the activity of cell enzymes was similarly changed. It is assumed that cellular manifestations of tolerance are the cause of reduced resistance of tolerant mice to ascitic carcinoma.