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Biomedical subjects

V V Khozinskiĭ

Publications and source records attributed to V V Khozinskiĭ.

At least 19 recordsLinked to original sources
PubMed1992

[The protective activity of preparations made from the tick-borne encephalitis virus grown using different cell cultures].

The preparations of tick-borne encephalitis (TBE) virus grown in swine embryo kidney cell culture have been shown to possess pronounced protective activity per unit of virion protein E in comparison with TBE virus preparations derived from cell culture 4647 and chick embryo cell culture. The antigenic activity of all virus preparations under study has proved to be practically the same. The role of post-translation modifications of TBE virus protein E in the manifestation of some of its biological properties is discussed.

Animals↗
PubMed1989

[Antibody-dependent harmful effect of non-immune spleen cells in acute experimental tick-borne encephalitis in mice].

The injection of nonprotective dilutions of immune serum and nonimmune spleen cells into mice infected with tick-borne encephalitis virus induced a sharply pronounced immunopathological effect: the mean survival time of the recipients decreased by 3.6 days in comparison with the control animals. This effect was not linked with the increased replication of the virus in the brain. The antibody-dependent damaging action of spleen cells could be reproduced by using the cells of both syngeneic and allogeneic donors. This phenomenon developed only in those cases when antibodies to the infective agent under study were used. The combination of immune serum to Japanese encephalitis virus and nonimmune spleen cells produced no damaging effect. The hypothesis stating that the antibody-dependent damaging action of nonimmune spleen cells arises from the antibody-dependent cytotoxic action of immunocompetent cells on the infected cells of the central nervous system is discussed.

Acute Disease↗
PubMed1987

[Role of antigen-nonspecific suppressors occurring in stress in the pathogenesis of Langat virus infection in mice].

Stress factors of different nature activate antigen-nonspecific suppressors inhibiting different mechanisms of immune response in mice. The adoptive transfer of the population of immunocompetent cells containing stress-induced suppressors to mice infected with Langat virus has been found to lead to the activation of asymptomatic infection. The data obtained in this investigation indicate that the above-mentioned mechanism of the development of antigen-nonspecific immune deficiency is of importance in the pathogenesis of viral infections in man and it explains the onset of diseases (or their aggravation) under the conditions of stress.

Animals↗
PubMed1986

[Study of immunological mechanisms of action of temperature and emotional stress factors in experimental flavivirus infections].

The influence of two stress factors, sharp changes in temperature and hypokinesia, on the course of experimental tick-borne encephalitis and Langat virus infections in mice has been studied. The data obtained in this study indicate that both factors produce defects in T- and B-cell-mediated immunity, accompanied by the activation of asymptomatic infection and the decrease of the mean survival time in acute infection. These two stress factors, differing in their intensity and nature (physical and emotional), have been shown to produce the same effect on the course of acute and asymptomatic flavivirus infections. In the former case the mean survival time of the animals decreases, and in the latter case clinically manifest infection develops. Under the conditions of hypokinesia (or changes in temperature), the death rate among the animals infected with langat virus has been found to increase 3- to 4-fold in comparison with the controls, the mortality level in the groups subjected to different stress factors being the same.

Animals↗
PubMed1985

[Role of virus-induced autoreactive T-lymphocytes, T-suppressors and the serum factor regulating their activity in the pathogenesis of experimental infection caused by the Langat virus in mice].

The precursors of autoreactive T-lymphocytes (PARTL) have been detected in the spleen of mice infected with Langat virus. When introduced into syngeneic recipients, PARTL differentiate in their lymph nodes into autoreactive T-lymphocytes (ARTL) causing a fatal autoimmune disease in the syngeneic recipients in vivo and capable of destroying syngeneic cell cultures in vitro. In the thymus of mice infected with Langat virus T-suppressors (TS) inhibiting the differentiation of PARTL into ARTL have been detected. The serum of intact mice has been shown to contain the serum blocking factor (SBF) which suppresses the differentiation of PARTL and the activity of TS from donors having common H-2 haplotypes of the gene complex with serum donors. In the course of viral infection the decrease of SBF activity and, simultaneously, the activation of PARTL and TS occur. The activation of PARTL and TS in infected mice may be suppressed by the injection of the serum of intact donors identical in H-2 haplotypes. The injection of ARTL induced by Langat virus into syngeneic recipients infected with this virus provokes the transformation of asymptomatic infection into acute infection, while TS and SBF blocking the differentiation of PARTL protect the animals from death.

Animals↗
PubMed1984

[Effectors of in vivo delayed hypersensitivity in experimental flavivirus infections and vaccination against tick-borne encephalitis in mice].

The development of experimental infections caused by tick-borne encephalitis (TBE) virus, Langat virus and dengue virus type 2 in mice or the immunization of these animals with live yellow fever vaccine (prepared from strain 17D) and inactivated TBE vaccine were accompanied by the formation of delayed hypersensitivity (DH) to viral antigens, determined in vivo. In experimental TBE infection the effectors of DH were identified as T-lymphocytes whose action was specific and followed the rule of H-2 restriction. The T-effectors of DH, induced by inactivated TBE vaccine, had no cytotoxic effect on an infected syngeneic tissue culture and, after their adoptive transfer by intravenous injection in vivo, did not protect syngeneic recipients against TBE virus.

Animals↗
PubMed1983

[In vitro study of macrophage barrier function in mice vaccinated against tick-borne encephalitis and infection with flaviviruses of varying virulence].

Tick-borne encephalitis (TBE) and Langat viruses were shown to be equally capable of multiplication in mouse peritoneal macrophages (PM) in vitro. The reproduction dynamics of TBE virus proved to be the same in PM of mice both highly sensitive and relatively less sensitive to TBE virus. The preliminary immunization of PM donors with commercial inactivated or experimental concentrated TBE virus vaccine produced no effect on the capacity of the virus for multiplication in PM. These facts indicate the absence of correlation between the capacity of the viruses under study for multiplication in PM in vitro and their virulence in vivo, as well as the insignificant role of circulating macrophages in the realization of the barrier function in an immune or nonimmune body.

Animals↗
PubMed1982

[Characteristics of bunyavirus- and togavirus-induced nonspecific suppressors inhibiting delayed hypersensitivity].

Some properties and mechanisms of action of nonspecific suppressor cells, inhibiting delayed hypersensitivity to sheep red blood cells and activated in vivo in experimental tick-borne encephalitis and Tahyna virus infections in mice, have been studied. These nonspecific suppressor cells have been identified as T-lymphocytes in experiments with the use of antisera to T- and B-lymphocytes. The function of the suppressor cells can be realized without their proliferation and is mediated by a soluble factor whose formation requires the synthesis of protein. In respect to hydrocortisone, the above-mentioned suppressor cells are subdivided into 2 subpopulations: hydrocortisone-resistant in the thymus and hydrocortisone-sensitive in the spleen.

Animals↗
PubMed1982

[Mechanisms of in vivo suppressive effect of togaviridae and bunyaviridae on the activity of effectors of graft vs host reaction].

Experiments on mice demonstrated the ability of 3 flaviviruses and 1 bunyavirus to suppress the activity of the effectors of the graft-versus-host (GVH) reaction. The conditions of the suppression of the primary immunological recognition were shown to differ in infections caused by different viruses. In experimental flavivirus infections caused by Langat, dengue 2 or yellow fever (strain 17D) viruses T-suppressor cells were activated, and their activity was realized only in respect to syngeneic or semisyngeneic target cells. In mice infected with Tahyna virus (a bunyavirus) no suppressor cells capable of suppressing the activity of the effectors of the GVH reaction were detected. The suppression of this reaction, not linked with the activity of the detected T-suppressor cells, was observed in the Langat virus infection under conditions of bilateral incompatibility when both the donor and the recipient were infected.

Animals↗
PubMed1980

[Protective and damaging action of cytotoxic T-lymphocytes in experimental tick-borne encephalitis].

The methods of adoptive transfer in vivo and cytotoxic action on virus-infected tissue culture in vitro were used to prove that cytotoxic splenocytes produced in experimental tick-borne encephalitis could have both protective and damaging effects. The protective effect was manifested during the first 24 hours after infection, and the damaging effect on the 6th day after infection. Cytotoxicity splenocytes were identified as T lymphocytes on the basis of their sensitivity to anti-theta serum, resistance to the action of hydrocortisone and their inability to adhere to glass, as well as their pronounced specificity and their limited activity in the allogeneic system.

Animals↗
PubMed1977

[Protective effect of cellular immunity in experimental Flavivirus infections].

Experiments were conducted with the tick-borne encephalitis (TE) virus; confirmation of a protective action of cellular immunity in mice was obtained. Administration of sensitized splenocytes to the animals together with the virus was accompanied with an increase of their mean survival or with the reduction of mortality in comparison with control animals given nonimmune or destroyed cells. The protective action of the effector cells was not connected with the intensification of antibody formation in the recipients. A high specificity of cellular immunity was noted in experimental flaviviral infections. The presence of common antigens in the TE and Langat viruses was revealed with the acid of cross splenocyte migration inhibition test (CSMRT). There was also revealed a difference of these viruses from the viruses of yellow fever, Dengue type 2, or Sindbis. The results of studying of the specificity of cellular immunity in the CSMRT found confirmation in experiments with adoptive transfer of splenocytes. Cross protection was caused only by splenocytes sensitized to the TE and Langat viruses.

Animals↗
PubMedDate not supplied

[2 aspects of immunity in experimental flavivirus infections].

Experimentally, two aspects protective and damaging, of the immune response were demonstrated in the course of development of infection in mice inoculated with tickborne encephalitis (TBE) virus, Langat, yellow fever, dengue type 2 or West Nile viruses. The experiments were carried out in animals in which the functions of T- and B-lymphocytes, were temporarily inhibited with cyclophosphane (CP). It was demonstrated that the protective or damaging role of the immune response depended on the method of inoculation of the animals, the virus properties, and characteristics of the mouse strain. The conditions optimal for the development of immunopathological reactions in one infection (TBE) were not identical for those in another infection even when caused by an antigenically related virus (LANGAT). In mice of the AKR strain the possibility of producing a therapeutic effect upon treatment with CP of the animals inoculated with TBE virus was demonstrated.

Animals↗