[Increasing the effectiveness of using cell cultures].
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Biomedical subjects
Publications and source records attributed to V A Zuev.
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Experiments with three cell lines revealed that the scraplecontaining cerebral extract, obtained from preliminarily infected 6-month mice, sharply induced the cellular proliferation, which was registered yet in 3 days after incubation. However, the cerebral extract of healthy 6-month mice did not virtually influence the velocity of cells' reproduction in all three cultures. The authors suggest, with respect to published data and to their independently found research results, that the gliosis of primary importance in shaping up the pathomorphological alterations in the cerebral tissue in prion diseases of man and animal.
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The status of the interferon system and level of immunoglobulins were studied in C57BL6 mice with slow influenza infection. These mice showed signs of immunosuppression: low endogenous interferon production, synthesis of alpha- and gamma-interferon by splenocytes of these mice in vitro 4-8 times lower than by those of the controls, lower levels of IgG in the blood serum. These data indicate general suppression of humoral immunity.
The structural and functional changes in organs and tissues of 30 young mice born from mothers treated intravenously with irradiation-inactivated influenza virus were studied. A detailed morphological analysis showed that a single inoculation of pregnant females with inactivated influenza virus resulted in the progeny in morphological lesions in organs and tissues typical of slow influenza infection.
Sick infants born to mothers who experienced influenza during pregnancy were examined. The cerebrospinal fluid, serum and blood cells were collected from such children with signs of congenital immune deficiency and progressive pathology of the central nervous system. None of the specimens yielded infectious influenza virus, but by means of molecular hybridization virus-specific genetic sequences were found in small amounts in the cerebrospinal fluid and serum and in high concentrations in blood cells. Persistence of genes NP, M and H1 of influenza A/H1N1 virus was observed in the blood cells of one infant for 83 days (the observation period). At the same time, the lack of antibodies to viral M protein in serum of this baby was demonstrated by the immune blotting method.
Inoculation of virus-specific cytotoxic lymphocytes (CTL) to pregnant mice infected with influenza virus was shown to result in a decrease of infectious virus concentration in the lungs and blood of mice as well as in the placentas and fetuses. With an increase in the dose of inoculated CTL, however, premature deliveries with stillbirths were observed as well as deaths of the mice, the highest frequency of fetal deaths being observed after infection of pregnant mice in the first half of pregnancy. It is not excluded that maternal virus-specific CTL played a role in the formation of developmental abnormalities and immunodeficient states in newborns.
Morphometric evaluation of the thymus and spleen was used to characterize the complex immunological deficiency in suckling mice developing as a result of transplacental transmission of both live and inactivated influenza virus.
Using 51Cr isotope label it was demonstrated that a very low per cent of syngeneic lymphocytes derived from healthy donors and inoculated in the blood stream of uninfected or influenza virus-infected pregnant mice is found in fetuses before delivery. Similar results were obtained after inoculation of virus-specific cytotoxic lymphocytes (CTL) into uninfected pregnant mice. After inoculation into the blood stream of infected pregnant mice of virus-specific CTL their migration into fetuses before delivery increases, being most marked in 25-30% of mice. Intravenous inoculation of excess CTL (10(6) cells) to infected pregnant mice resulted in rapid development of signs of slow influenza infection in the progeny with typical clinical picture and histopathological lesions in organs and tissues. Large doses (10(7)-10(8) cells) of CTL inoculated into the blood stream cause higher reduction and death of fetuses and increase the rate of stillbirths. The role of maternal virus-specific CTL in the pathogenesis of experimental congenital and especially slow influenza infection is discussed.
It had previously been shown that intrauterine infection of mice with influenza virus resulted in growth retardation and significant immunosuppression to various nonspecific agents and influenza virus. The present study demonstrated that such mice also had lower production of specific antibody and reduced capacity to form the delayed hypersensitivity to influenza virus. Despite the lack of specific immune response, such mice had high levels of response to influenza virus in adoptive transfer. The reasons for which lymphocytes of mice with slow influenza infection fail to manifest their immunological potentials in situ require further study.