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Biomedical subjects

J C Overall

Publications and source records attributed to J C Overall.

At least 91 records · Page 5Linked to original sources
PubMed1975

Herpesvirus hominis infection in newborn mice: comparison of the therapeutic efficacy of 1-beta-D-arabinofuranosylcytosine and 9-beta-D-arabinofuranosyladenine.

Intranasal inoculation of newborn mice with Herpesvirus hominis type 2 provides an experimental infection that closely resembles disseminated herpesvirus infection of human newborn infants. After inoculation of mice, the virus multiplies in the respiratory tract and is disseminated through the blood to the liver and spleen and to the brain by both a viremia and nerve route transmission. Although therapy with 1-beta-d-arabinofuranosylcytosine (ara-C) did not reduce final mortality, it did increase the mean survival time by 1 day. This effect on the mean survival time was associated with a 1-day delay in the appearance of herpesvirus in the blood, liver, and spleen and a reduction of virus replication in lung and brain for 1 day as compared with untreated control animals. Treatment with 9-beta-d-arabinofuranosyladenine (ara-A) likewise had no effect on final mortality, but increased the mean survival time by 2 days. Therapy with ara-A delayed or suppressed virus replication in blood, lung, liver, spleen, and brain for 2 days. Although treatment with either ara-C or ara-A in this experimental H. hominis type 2 infection resulted in a temporary delay and/or suppression of viral replication in several target organs, neither compound was completely effective in inhibiting viral replication or in protecting animals from eventual death due to the infection.

Animals↗
PubMed1975

Herpesvirus hominis infection in newborn mice: treatment with interferon inducer polyinosinic-polycytidylic acid.

Intranasal inoculation of newborn mice with Herpesvirus hominis (HVH) type 2 provides a model for disseminated herpesvirus infections of human newborn infants. Treatment of this experimental infection with polyinosinic-polycytidylic acid [poly(I:C)] significantly increased the mean survival time and markedly altered the pathogenesis of the infection. No significant protection against final mortality was observed. Poly(I:C) therapy completely inhibited detectable viral replication in all target organs tested except the brain. In the brain there was a 2-day delay in the onset of viral replication in treated animals, which correlated with the 1- to 2-day increase in mean survival time. In general, the control of HVH replication occurred in those target organs in which poly(I:C)-induced interferon was detectable. The failure of poly(I:C) to alter the final mortality of newborn mice infected with HVH appears to be primarily due to the lack of sufficient levels of interferon induced in brain tissue and the failure to prevent viral replication in this critical target organ.

Animals↗
PubMed1975

Genital herpesvirus hominis infection in mice. I. Development of an experimental model.

Pregnant female mice, after intravaginal inoculation with Herpesvirus hominis (HVH) type 2, developed vaginitis on days 5 to 7 after virus challenge, followed by hunching and hind limb paralysis on days 7 to 9 and death from encephalitis on days 9 to 11. After initial replication in the mucous membranes of the genital tract, virus spread to the spinal cord and ascended to involve the brain. Viremia or replication of H. hominis type 2 in the liver or spleen was not detected. Virus was cleared from vaginal secretions by days 8 to 10 after infection. Pregnant mice were more susceptible to the infection than nonpregnant mice. This experimental infection in female mice provides a model for genital herpesvirus infection and for herpesvirus infection and for herpesvirus encephalitis in which one can evaluate potentially promising antiviral chemotherapeutic agents.

Animals↗
PubMed1975

Viral replication and interferon production in fetal and adult ovine leukocytes and spleen cells.

Peripheral blood leukocyte and spleen cell cultures derived from adult sheep and from third-trimester (107 to 145 days of gestation) and second-trimester (70 to 98 days of gestation) fetal lambs were examined for their ability to support viral replication and to produce interferon. Bluetongue virus, Herpesvirus hominis type 2, and Chikungunya virus failed to replicate in either leukocyte or spleen cell cultures derived from adult ewes or in cultures from second- or third-trimester fetal lambs. Similarly, peripheral blood leukocytes from adult sheep or third-trimester fetal lambs did not support the replication of Semliki Forest virus, vesicular stomatitis virus, Newcastle disease virus, or vaccinia virus. No major differences were observed in the ability of fetal and adult leukocytes to produce interferon in response to viral infection. In contrast, mean interferon titers induced by bluetongue virus, H. hominis type 2, and Chikungunya virus in spleen cells from second-trimester fetuses were 4- to 10-fold greater than those induced in spleen cells from adult ewes. Variations in interferon levels induced on separate occasions with cells from the same donor age group were observed. The antiviral substance induced in both the fetal and adult cell cultures fulfilled the usual criteria for characterization as interferon.

Aging↗
PubMed1975

Mycoplasma-mediated hyporeactivity to various interferon inducers.

Three strains of Mycoplasma arthritidis were shown to induce marked hyporeactivity in mice to interferon induction by both Newcastle disease virus and poly(I:C). In contrast, the interferon response of mice to tilorone was only partially suppressed by pretreatment of the animals with mycoplasms. Hyporeactivity to Newcastle disease virus was maximal 1 and 3 days after mycoplasms treatment, but the interferon response was maximal 1 day after injection of the mycoplasmas and was no longer apparent by 5 days. No relationship was found between the ability of the mycoplasms themselves to induce interferon and the degree of hyporeactivity produced. These results suggest that mycoplasmas may alter virus-host relationships in vivo.

Animals↗
PubMed1974

Induction of interferon in mice by mycoplasmas.

Interferon was induced in mice after intraperitoneal inoculation with four different mycoplasmas. Peak levels of between 100 and 300 U of interferon per ml were attained by 6 h postinfection with each of the mycoplasmas except Mycoplasma arthritidis, which induced higher titers (400 to 11,800 U/ml) by this time. A fifth mycoplasma, M. pulmonis, induced interferon inconsistently and at a later (72 to 96 h) time. Mycoplasmatales virus MVL51 and sterile mycoplasmal broth did not stimulate interferon production in vivo. All of the mycoplasmas and MVL51 failed to induce interferon in murine spleen cell, peritoneal exudate cell, or peripheral blood leukocyte cultures. Preinfecting the mycoplasmas with MVL51 or treating the organisms with trypsin or dilutions of specific antisera did not enhance their ability to induce interferon in vitro.

Acholeplasma laidlawii↗
PubMed1973

Mycoplasma-associated induction of interferon in ovine leukocytes.

A mycoplasmal species, Acholeplasma laidlawii, isolated as a contaminant from a fetal lamb kidney cell line, was shown to be associated with the induction of interferon in cultures of ovine peripheral blood leukocytes. Broth cultures of the mycoplasma induced between 20 and 230 U of interferon per ml in leukocytes from two adult ewes. The amount of interferon produced correlated with the inoculum size of mycoplasma. Interferon production was associated with replication of the mycoplasma in the leukocyte cultures. Interferon was not induced by sterile mycoplasmal broth, a cell-free filtrate of the mycoplasmal cultures, or heat-inactivated mycoplasmas. The antiviral substance was characterized as interferon by the usual criteria.

Animals↗
PubMed1970

Fetal response to viral infection: interferon production in sheep.

When virus was inoculated intravenously during the third trimester, the gestating ewe produced only low amounts of serum interferon, whereas the fetal lamb had the capacity to produce extremely high amounts. There was no evidence of transplacental transfer of interferon between mother and fetus in either direction.

Animals↗