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Biomedical subjects

V V Khozinsky

Publications and source records attributed to V V Khozinsky.

10 recordsLinked to original sources
PubMed1990

Replication of Langat virus in immunocompetent cells of mice subjected to immobilization stress.

Immobilization stress (hypokinesis) in Balb/c mice may aggravate asymptomatic infection with Langat virus (strain TP-21) as evidenced by 4-fold increased lethality in comparison with control animals. The virus levels in the spleen and brain of stressed and infected mice and the in vitro yield of the virus in immunocompetent cells derived from stressed mice were significantly higher than in controls. Enhanced virus replication in latter cells may contribute to increased accumulation of the infectious agent in lymphatic tissues, which would facilitate virus invasion into CNS followed with acute disease and death of animals.

Animals↗
PubMed1986

H-2 restricted regulation by soluble autoantigens of the tick-borne encephalitis virus-induced autoreactive T-effector and T-suppressor lymphocytes in mice.

Soluble autoantigens (mouse red blood cells lysed by sonication) blocked in vitro the antigen-recognizing receptors of tick-borne encephalitis (TBE) virus-induced autoreactive T-lymphocytes (ARTL), effectors of the local graft-versus-host reaction (GVHR) in a syngeneic system and prevented the development of GVHR in vivo. Antigen-recognizing receptors were also found on T-suppressors (Ts) that became activated during experimental tick-borne encephalitis in mice and inhibited the activity of ARTL. The interaction between these receptors and autoantigens in vitro resulted in a loss of the ability of Ts to inhibit in vivo the ARTL-mediated GVHR. A similar result was obtained with ARTL and Ts activated in mice infected with Langat, dengue type 2 (D2) and yellow fever (strain 17D) viruses. The block of the antigen-recognizing receptors of T-cells was reversible, and not associated with lymphokine production or effector death. The block of the antigen-recognizing receptors in vitro and the loss of the corresponding T-cell function in vivo occurred provided that the donors of soluble erythrocyte antigens (SEA) and of the lymphocytes had at least one common major histocompatibility complex (MHC) haplotype. Injection SEA from donors whose H-2 complex haplotypes were identical to those of TBE-infected recipients prevented in the latter the formation of ARTL or Ts. The autoantigens inhibiting the ARTL and Ts activities seemed to be products of the MHC genes. The role of soluble H-2 autoantigens in preventing virus-induced autoimmune reaction and maintaining a state of natural immunological tolerance is discussed.

Animals↗
PubMed1985

Virus-induced decrease in the activity of serum blocking factor(s): a mechanism of activation of the autoreactive T effectors in graft versus host reaction and of controlling T suppressors.

It has been shown that serum blocking factor(s) (SBF) previously detected in normal mice bind(s) to receptors on the surface membranes of virus-induced autoreactive T lymphocytes (ARTL) and to that of ARTL activity inhibiting T suppressors (TSar). The interaction of SBF with the receptors is reversible, H-2 restricted and associated with the inhibition of functional activity of the tested T lymphocyte populations. In mice during acute tick-borne encephalitis (TBE), in the course of inapparent infections induced by Langat virus or dengue type 2 (D2) and after infection with the attenuated yellow fever virus (strain 17D), the SBF activity significantly decreased, while ARTL and TSar became activated. Administration of normal mouse serum to infected animals with SBF deficiency resulted in inhibition of both inductive and productive phases of ARTL and TSar formations. Based on these findings, the virus-induced decrease in SBF activity may be considered as one of the mechanisms triggering autoimmune responses. The autoreactive pathological states can develop under various endo-and/or exogenic conditions influencing on SBF and on the TSar activity.

Animals↗
PubMed1985

Role of macrophages in the pathogenesis of experimental tick-borne encephalitis in mice.

In vivo phagocytosis activity of macrophages (PAM) was temporarily suppressed in mice by application of a suspension of microscopic from particles. As demonstrated, a reversible block of 70% of PAM was accompanied by a marked increase of the lethality during the acute tick-borne encephalitis (TBE) virus infection. Asymptomatic persistence of TBE virus in the brain was 4 times more frequent in mice with PAM defect than in immuno-competent mice. Suppression of PAM during the first 48 hr post infection (p.i.) did not affect interaction of B-, T-lymphocytes and macrophages. Cytotoxic activity of splenocytes against TBE virus-infected mouse embryo fibroblasts (MEF) was alike irrespective of whether cytotoxic cells were collected from mice inoculated or not inoculated with microscopic iron suspension. Similarly, frequency of seroconversion did not differ in these groups of mice. Adoptively transferred peritoneal macrophages from TBE virus-infected or intact mice did not exert any protective activity. The presence of splenic macrophages was necessary neither in adoptive immunity transfer in vivo nor in cytotoxic activity of T-lymphocytes directed to virus-infected targets in vitro. It was further found that peritoneal macrophages (PM) both from TBE virus immunized and non immunized donors in the presence of antibodies to TBE virus acquired the capability to kill TBE virus-infected target cells. Antibody-dependent cytotoxicity (ADC) of macrophages was associated with population of phagocytic cels.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Variability of Powassan virus cultured in tissue explants and organism of Hyalomma anatolicum ticks.

The variability of Powassan virus was studied during successive passages in Hyalomma anatolicum ticks or prolonged reproduction in their tissue explants. It had been shown that in the course of tick passages and during reproduction in the explants, pathogenicity of the virus in respect to causing acute disease in mice after peripheral inoculation was decreased, while virus ability to cause death after intracerebral (i.c.) inoculation remained unchanged. In mice infected with the original strain P-40 of Powassan virus damaging effect of the immune response prevailed, while in mice infected with the strains passaged for a long time in ticks (strain P-40Hat) or in tick tissue explants (strain P-40Haex), the protective effect of the immune response was prominent.

Animals↗
PubMed1984

In vivo inhibition by intact mouse serum of the activity of the flavivirus-induced T-suppressors of autoreactive T-lymphocytes.

In the serum of healthy mice a factor was found inhibiting the in vivo effect of T-suppressors of autoreactive T-lymphocytes (TSart1) induced in mice by tick-borne encephalitis (TBE) virus, Langat virus, dengue virus type 2 (D2) and attenuated strain 17D of yellow fever virus. Activity of the serum factor (s) was demonstrated providing that the TSart1 had H-2 antigens completely or partially identical with the H-2 antigens of serum donors. The activity was not connected with destruction of TSart1. The factor (s) did not inhibit the in vivo activity of TBE virus-induced T-suppressors directed to the effectors of graft versus host reaction (GVHR) in allogeneic mice. These suppressors differed from TSart1 in their distribution in the organs of immune system. As suggested, the serum factor (s) inhibiting TSart1 may be involved in pathogenesis of virus infections and in regulation of virus-induced autoimmune processes.

Animals↗
PubMed1983

Serum factor blocking the activity of virus-induced autoreactive T lymphocytes of mice.

Normal mouse serum was found to contain a factor blocking in vivo the effect of autoreactive cells accumulating in spleens of mice infected with tick-borne encephalitis (TBE), Langat, dengue type 2 (D2), and attenuated yellow fever (17D strain) viruses. The activity of the factor was manifested only, when the autoreactive lymphocytes had H-2 antigens identical with H-2 antigens of the serum donors. The hypothesis is discussed that serum factor protects the host against clones of autoreactive T lymphocytes generated in viral infections.

Animals↗
PubMed1981

Nonspecific T-suppressors in experimental tick-borne encephalitis.

Suppressor cells inhibiting graft-verus-host reaction under conditions of two-way incompatibility were activated in lymphoid organs of tick-borne encephalitis virus-infected mice. Cells with suppressor activity were found in the thymus, peripheral lymph nodes (LN) and spleen but not in the bone marrow, or peritoneal exudate cells adhering to the plastic surface. The cells were identified as T lymphocytes based on the following properties: sensitivity to anti-theta serum, inability to adhere to plastic surface, and resistance to anti-mouse gamma-globulin serum. The T suppressors were activated 3 days after infection (p. i.) in the thymus and LN and at 4 days in the spleen; they were detectable until the appearance of clinical signs of the disease (8-9 days p. i.).

Animals↗
PubMed1975

The damaging action of cellular immunity in flavivirus infections of mice.

The development of acute infections caused by different flaviviruses was studied in immunosuppressed inbred and non-inbred mice. Cyclophosphamide treatment of challenged animals resulted in an increase of the mean survival time by 24--144 hours in some but not all virus-mouse strain combinations. The transient protective action of cyclophosphamide was not due to suppression of the reproduction of tick-borne encephalitis (TBE) or dengue 2 (D2) virus in the brains of mice. In TBE or D2 infections of immunosuppressed mice the clinical signs of central nervous system lesions seemed to be associated with the development of cellular immunity measured by the splenobyte migration inhibition test. The transfer of sensitized splenocytes in immunosuppressed animals, challenged with TBE or D2 virus, shortened the incubation period. These results suggest that cellular immunity may have a damaging effect in acute flavivirus infections in mice, and also that the immunopathological response varies considerably in different strains of inbred mice.

Acute Disease↗