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Biomedical subjects

L M Farutina

Publications and source records attributed to L M Farutina.

12 recordsLinked to original sources

Chronic alphavirus infection of L cells.

Chronic infection of L cells with Sindbis virus, induced in the absence of antiviral antibody, was studied by virological methods in combination with light and electron microscopy. Both Sindbis virus and endogenous oncovirus antigens were revealed in the cells by immunofluorescence. Sindbis virus and interferon were detected in the culture fluid. Immunoelectron microscopy revealed aggregation of Sindbis virus particles by immune serum.

Antigens, Viral↗

[Pathology and immune lysis of cells infected with measles virus isolated from subacute sclerosing panencephalitis].

The Si strain isolated from a patient with subacute sclerosing panencephalitis like reference measles virus strains was shown to induce in cell cultures formation of symplasts and spindle-shaped cells, cytoplasmic and intranuclear inclusions, pathology of mitosis, appearance of intracellular and surface virus-induced antigens. The presence of the latter caused cell cytolysis under the effect of measles immune sera and complement.

Antigens, Viral↗

[Dependence of immune cytolysis of cells infected with western equine encephalomyelitis virus upon the cell cycle stages].

In the first few hours after inoculation of Chinese hamster cells with western equine encephalomyelitis virus the mitotic activity of the cells did not change significantly but mitoses stopped mainly in the stage of metaphase and had all signs of pathological mitoses. Treatment of the cells for 1 hour with the homologous antiviral immune serum and complement resulted in destruction and death of practically all cells except those in the state of mitosis. In the latter specific fluorescence of virus antigen was demonstrated by the fluorescent antibody technique same as before treatment with the homologous immune serum and complement. Resistance of mitoses to immune cytolysis is probably conducive to virus persistence.

Animals↗

[Change in the nature of the persistence of alpha- and flaviviruses in the body of BALB/c strain mice with a mixed infection with leukovirus].

The features of pathogenesis of infection caused in adult Balb/c mice intraperitoneally infected with Sindbis virus, virulent or attenuated strains of West Nile (WN) virus, individually or in combination with Rauscher leukemia virus (RLV) were studied. The influence of the latter on the course of togavirus infections was characterized by 3 features: (a) different effects on the visceral and neural phases of the pathogenesis (increased period of viremia and virus reproduction in the viscera did not lead to stimulation of virus reproduction in the CNS); (b) changes in the time of togavirus persistence in the infectious form; (c) the dependence of the observed effect on the togavirus properties.

Animals↗

[Mechanisms of the stimulating action of the Rauscher leukemia virus on togavirus reproduction in the bodies of BALB/c strain mice].

Reciprocal stimulation or inhibition are observed in double infection of mice with Rauscher leukemia virus (RLV) and togaviruses Sindbis or West Nile (WN). Stimulation of togavirus infections is manifested by the enhancement of the visceral phase of pathogenesis without subsequent activation of togarivus reproduction in the CNS. This effect is accompanied by enhanced togavirus replication in splenocytes, a decrease in the number of antibody-producing cells in the spleen, a decrease of antihemagglutinins titer in the blood without any significant change in the virus-neutralizing antibody and interferon titers. RLV-induced immunosuppression is termporary and of varying intensity with regard to individual parameters of immune response and to different variants of WN virus (highly virulent, poorly virulent). It is assumed that the differentiated and temporary nature of the immunosupressive effect of RLV is conducive to selective stimulation of the visceral phase of togavirus reproduction followed by inhibition of the neural phase under the influence of restored immune mechanisms and interferon. Because of the defects of humoral and cellular immunity, however, no complete elimination of togavirus occurs and conditions for its long-term persistence are created.

Animals↗