Studies on the Pathogenicity of Human‐Origin Parainfluenza Virus in the Brain of Mice

Shimokata, Kaoru

doi:10.1111/j.1348-0421.1978.tb00401.x

Cited by 19 publications

(6 citation statements)

References 20 publications

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“…Interferon titration. Interferon was assayed by the cytopathic effect inhibition microassay method with mouse L cells and vesicular stomatitis virus as the challenge virus (8). The reciprocal of the highest dilution of the sample causing 50%o protection was taken as the interferon titer.…”

Section: Methodsmentioning

confidence: 99%

Component(s) of Sendai virus that can induce interferon in mouse spleen cells

Ito¹,

Hosaka²

1983

Infect Immun

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To identify the active component of Sendai virus that induces interferon in mouse spleen cells, infectious and noninfectious viruses, envelope particles derived from them, and isolated hemagglutinin-neuraminidase (HN) glycoproteins were examined for interferon induction. The interaction between membranous structures containing Sendai virus HN glycoprotein and the receptors on the cell surface was shown to be sufficient for interferon induction in mouse spleen cells, suggesting that the actual inducer of interferon in mouse spleen cells is the HN glycoprotein of Sendai virus. When mouse spleen cells were stimulated in vitro with Sendai virus grown in eggs or LLC-MK2 cells or with membranous structures containing glycoproteins obtained from these viruses, interferon could be detected in the culture fluid. Furthermore, isolated HN glycoprotein per se could induce interferon in the cells. A linear correlation was found between the titer of interferon induced and the hemagglutinating activity of the membranous structure containing the HN glycoprotein. It was concluded from these findings that HN glycoprotein was the active component of Sendai virus responsible for interferon induction in mouse spleen cells and that viral RNA and F glycoprotein were not required. The results also showed that the interaction between HN glycoprotein and receptors on the cell surface triggered production of type I interferon (IFN-alpha and IFN-beta). Although when Sendai virus was incubated at 56 degrees C for 5 min it lost its hemolytic and hemagglutinating activities, it induced a considerable amount of interferon in the culture fluid of mouse spleen cells. The interferon-inducing ability of heat-inactivated virus could be absorbed with mouse spleen cells but not with sheep erythrocytes or mouse erythrocytes, indicating that the inactivated virus retained ability to bind to mouse lymphoid cells.

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Section: Methodsmentioning

confidence: 99%

Component(s) of Sendai virus that can induce interferon in mouse spleen cells

Ito¹,

Hosaka²

1983

Infect Immun

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“…Interferon titration. Interferon was assayed by the cytopathic effect (CPE)-inhibition microassay method with mouse L cells and vesicular stomatitis virus as challenge virus (21). The highest dilution of the titrated sample causing at least 50% protection was considered the end point.…”

Section: Methodsmentioning

confidence: 99%

Immune Interferon Produced In Vitro as a Quantitative Indicator of Cell‐Mediated Immunity

Ito

Nishiyama

Shimokata

et al. 1979

Microbiology and Immunology

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The present study was constructed to provide some information on the possibility of utilizing immune interferon as a quantitative indicator of cell-mediated immunity and to clarify some of the nature of immune interferon-producing cells (IIPC).When spleen cells derived from L cell-sensitized mice were co-cultivated with L cells, interferon appeared in the culture fluid. It was shown by additional experiments that the cells responsible for immune interferon production in this system were T-lymphocytes assisted by macrophages. The pattern of kinetics of immune interferon production in vitro was similar to that of migration inhibitory factor or T cell-mediated cytotoxicity.

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“…Interferon (IFN) titers in lung homogenates were determined by the procedure of Shimokata [12] using vesicular stomatitis virus and L929 cells. Mumps virus in the samples was neutralized by anti-mumps virus serum prior to IFN titration.…”

Section: Interferon Assaymentioning

confidence: 99%

Replication of mumps virus in mouse: transient replication in lung and potential of systemic infection

Tsurudome

Yamada

Hishiyama

et al. 1987

Archives of Virology

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A mumps virus strain, which replicated in mouse lung after aerosol inhalation, was obtained by selective replication of a wild strain in L929 cells and by further passaging in mice by intraperitoneal inoculation. All of infected mice survived and rechallenge of the survived mice with the same virus resulted in no virus growth in the lung. Treatment of infected mice with antiserum against interferon (IFN) or asialo GM1 delayed virus clearance from lung. Mice at 5 weeks of age were also sensitive to the virus as well as those at 1 week. When injected intravenously, the virus could grow not only in lung but also in salivary glands, heart and spleen. Furthermore, the virus replicated in liver, spleen, pancreas and testis after intraperitoneal inoculation. Antibody response of mice infected by aerosol inhalation was slower than that of intraperitoneally infected ones in either IgG or IgM production. These results indicated that the adapted virus replicated in mouse lung by a natural route of infection and had a potential to cause systemic infection in mouse.

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Studies on the Pathogenicity of Human‐Origin Parainfluenza Virus in the Brain of Mice

Cited by 19 publications

References 20 publications

Component(s) of Sendai virus that can induce interferon in mouse spleen cells

Component(s) of Sendai virus that can induce interferon in mouse spleen cells

Immune Interferon Produced In Vitro as a Quantitative Indicator of Cell‐Mediated Immunity

Replication of mumps virus in mouse: transient replication in lung and potential of systemic infection

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