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Biomedical subjects

J Booss

Publications and source records attributed to J Booss.

At least 37 records · Page 2Linked to original sources
PubMed1986

Inbred guinea pig model of intrauterine infection with cytomegalovirus.

Outbred guinea pigs have previously been utilized in an experimental model for the study of congenital infection with cytomegalovirus (CMV). Development of an inbred model of intrauterine CMV infection would allow analysis of the cells involved in CMV immunity, studies of transplacental CMV transfer, and investigation of the cellular immune factors that participate in intrauterine CMV infections. This study was therefore designed to assess the inbred guinea pig as a model for the study of congenital CMV infection. Intrauterine fetal and placental infection with CMV was demonstrated in inbred Strain 2 guinea pigs, and the maternal factors influencing transplacental transmission of CMV were evaluated. Infectious virus was recovered from placentas and offspring of mothers that experienced primary CMV infection during pregnancy, but not from placentas and offspring of mothers that were inoculated with CMV prior to pregnancy. However, histologic lesions consisting of focal necrosis and inflammation were seen in tissues of offspring from both groups of mothers. Inoculation of seronegative pregnant Strain 2 animals with low doses of virus (2.5 to 3.5 log10 TCID50) resulted in both placental and fetal CMV infection without significant maternal death. Infection of placentas and offspring occurred in utero regardless of the stage of pregnancy. In addition, infectious virus was detectable in fetal tissues at the time of maternal viremia but also later during the course of maternal infection, ie, 4 weeks after inoculation. These findings indicate that the inbred guinea pig model can be used to investigate the pathogenesis of intrauterine CMV infections.

Animals↗
PubMed1985

Human eastern equine encephalitis. Electron microscopic study of a brain biopsy.

An electron microscopic study was done on brain biopsy tissue from an eight-month-old female with acute eastern equine encephalitis diagnosed by indirect immunofluorescence. Rare clusters of round virions were found almost exclusively in the extracellular space. All virions observed had spiked envelopes, and their sizes averaged approximately 55 nm. Also found were rare enveloped virions along with degenerate organelles in a membrane-bound structure in the cytoplasm of macrophages. Intracytoplasmic development of virions was not found. Tubuloreticular complexes were seen in the endothelial cells and macrophages. This is the first report of an electron microscopic study on biopsy material from a case of human eastern equine encephalitis. It will extend the usefulness of brain biopsy in the diagnosis of acute encephalitis.

Astrocytes↗
PubMed1985

Delayed contralateral hemiplegia following herpes zoster ophthalmicus: should antiviral therapy be used?

We review clinical virological studies in the syndrome of delayed contralateral hemiplegia following herpes zoster ophthalmicus. Virus could not be isolated from the cerebrospinal fluid (CSF) of the present case, nor was antiviral antibody found in the CSF. There appear to have been no reports of successful virus isolation from the CSF although there are reports of antibody in the spinal fluid. Thus the evidence for ongoing viral replication in the central nervous system is marginal. It is suggested that the sensitive antibody assay against membrane antigens (FAMA) be used in the future as a guide to antiviral therapy.

Adult↗
PubMed1984

Asynchronous depression of responses to T- and B-cell mitogens during acute infection with cytomegalovirus in the guinea pig.

The nonspecific functional capacity of spleen cells, taken from female guinea pigs with primary acute cytomegalovirus (CMV) infection, was assessed using lipopolysaccharide (LPS), a B-cell mitogen, and concanavalin A (Con A), a T-cell mitogen. Proliferative responses to the two mitogens were found to be significantly depressed in animals inoculated with CMV as compared to control animals. The defect in Con A responsiveness occurred earlier during the course of the infection than the defect in LPS responses. Although responses to the mitogens were depressed at the time of peak virus activity in the spleen, the possibility of lytic destruction of the spleen cells by the virus during in vitro culture was excluded. In addition, the depression in Con A responsiveness was noted with a wide range of Con A concentrations, and preculture studies failed to result in enhanced reactivity of the cells from infected animals. We conclude that reductions of both B- and T-cell functions, which differ in their timing during the course of acute CMV infection, occur concurrently with an enhanced viral specific immune response in guinea pigs acutely infected with CMV.

Animals↗
PubMed1984

Comparison of methods to identify microglial cells and macrophages in the human central nervous system.

The macrophage markers non-specific esterase, alpha 1-antitrypsin, alpha 1-antichymotrypsin, and lysozyme were compared with conventional microglial and macrophage stains in the human central nervous system. In a series of specimens from cases of head trauma, conventionally fixed and embedded, the modified Weil-Davenport stain was unequivocally best for demonstrating reactive microglia. alpha 1-antichymotrypsin, however, was the most effective for showing macrophages in a series of specimens from patients with other conditions, which included inflammatory, neoplastic, and non-inflammatory diseases. The non-specific esterase reaction was unsatisfactory in tissues fixed in neutral formalin but was successful in fresh frozen tissue. In a series of specimens from cases of multiple sclerosis, non-specific esterase showed demyelination clearly and stained neuronal cytoplasm. It also stained macrophages but was less satisfactory for lipid-bearing phagocytes in multiple sclerosis than oil red 0.

Brain Injuries↗
PubMed1983

Immunohistological analysis of T lymphocyte subsets in the central nervous system in chronic progressive multiple sclerosis.

In an analysis of pooled data, we have found that cytotoxic-suppressor T cells outnumber the helper-inducer subset and also the population of cells bearing the pan-T cell marker in specimens of CNS from patients dying with MS (Booss et al. 1983). In the present study of individual data, we have reviewed the case histories to determine if these findings were consistent in various clinical settings. Variables examined included disease duration, tempo of evolution, immunosuppressive therapy, and other potentially immunomodulating features such as tumours. The predominance of the cytotoxic-suppressor subset was not found to be altered by any of these variables. We also present an individual data analysis of cases dying without known CNS disease and of cases with chronic non-inflammatory CNS disease. We found that the low but consistently observed number of T cells was apparently unrelated to the age of the individual or the site of the CNS sampled. Analysis of selected perivascular infiltrates showed, in contrast to the CNS parenchyma, that the pan-T cells and each of the subsets were approximately equal in proportion. Consideration of this observation and of the cytotoxic-suppressor subset preponderance in the parenchyma is compatible with the possibility of antigenic modulation of the T cell differentiation antigens. Finally, the potential contribution of perivascular infiltrates to the CSF pleocytosis is considered.

Aged↗
PubMed1983

Herpes simplex encephalitis: analysis of a cluster of cases by restriction endonuclease mapping of virus isolates.

In December 1979, there were three deaths from culture-proven herpes encephalitis in 3 weeks in the New Haven area, and a nurse caring for one of these patients developed a herpetic lesion on her nose. The three brain isolates, the isolate from the nurse, and several epidemiologically unrelated strains were analyzed by restriction endonuclease mapping. All were determined to be distinct strains of herpes simplex virus. The possibility that a single strain of virus caused this cluster of cases was therefore examined directly and disproved.

Adolescent↗
PubMed1982

Duration of vidarabine therapy in biopsy-negative herpes simplex encephalitis.

Vidarabine therapy reduces mortality due to herpes simplex encephalitis (HSE) from 70% to 40% at one year. Treatment with vidarabine is commonly terminated five days after biopsy in suspected HSE if herpes simplex virus is not isolated from the biopsy specimen. However, as demonstrated by this case report, virus distribution in brain tissue may be patchy, even within the temporal lobe. In addition, several technical factors in the process of virus isolation can result in falsely negative results at five days. To protect this subgroup of patients with HSE, a full ten-day course of antiviral therapy should be considered for patients with focal encephalitis whose biopsy results are negative, provided that HSE remains the principal diagnostic possibility. However, the potential benefit of vidarabine treatment must be weighed against the risk of side effects, particularly cerebral edema. For optimum care, patients with presumed HSE should be transferred to centers whose personnel have expertise in the diagnosis and management of this disease.

Aged↗
PubMed1981

Immune stimulation, inflammation, and changes in hematopoiesis. Host responses of the murine spleen to infection with cytomegalovirus.

Spleens from C3D2F1 mice acutely infected with murine cytomegalovirus (MCMV) were examined for mechanisms of viral clearance and alteration of immune function. Inclusion-bearing cells in the perifollicular marginal zone were found to peak at Day 3 after infection and to be associated with infiltrates of polymorphonuclear leukocytes (PMNs). Inclusions and PMNs were cleared by Day 6. Hematopoietic islands, although not impinged upon, could not be found by Day 3 after infection but reappeared and were considerably enlarged by Day 6. Most importantly the T-dependent areas of the spleens revealed no viral inclusions and no lysis. Stimulated morphology was seen in T-dependent areas by Day 1 after infection and remained so for over 3 weeks. T-independent areas contained germinal centers at Day 4 and thereafter. Therefore, in the absence of viral cytopathologic features in the T-dependent and T-independent areas, other mechanisms must account for the immunosuppression observed during acute infection. The observations of an activated morphology are compatible with other data demonstrating an alteration in immunoregulation as the mechanism for the immunosuppression associated with MCMV infection.

Animals↗
PubMed1981

Adherent spleen cells from mice acutely infected with cytomegalovirus suppress the primary antibody response in vitro.

In the present study, we have demonstrated that the hemolytic plaque response of spleen cells from mice acutely infected with murine cytomegalovirus (MCMV) is suppressed in vitro. Mishell-Dutton cultures established with spleen cells from C57BL/6 mice infected 4 days earlier with 4.2 X 10(3) plaque-forming units of MCMV were found to produce significantly fewer direct plaques upon stimulation with sheep red blood cells than corresponding control cultures. Suppression could not be attributed to a generalized lytic destruction of spleen cells, nor was it produced by addition of virus directly to uninfected spleen cell cultures. However, in cultures containing various mixtures of cells from control and infected mice, the direct plaque response was markedly below the predicted response, suggesting that the uninfected cells were actively suppressed by cells from infected mice. Suppression was dependent on the presence of intact spleen cells, since it was not found in the presence of lysed cells. The capacity of spleen cells from infected mice to mediate suppression was demonstrated in the plastic-adherent subpopulation. Treatment of these cells with anti-thymocyte serum (ATS) and complement did not abolish the capacity to suppress the immune response. Thus, adherent ATS-resistant cells from the spleens of mice acutely infected with MCMV, rather than virus alone, have the capacity to actively suppress the hemolytic plaque response in vitro.

Animals↗
PubMed1980

Establishment of cytomegaloviral infection in mice: role of a macrophage-enriched subpopulation.

The role of a macrophage-enriched subpopulation in acute intraperitoneal infection of mice with cytomegalovirus was investigated. Virus was not detectable in extracellular fluid after the first day, but it could be isolated from peritoneal exudate cells for at least three weeks after infection. The virus was found in adherent and nonadherent cells after plastic-adherence separation. Infection of recipient mice was achieved by adoptive transfer of either subpopulation two or 21 days after infection. Further study of the macrophage-enriched adherent subpopulation revealed no evidence of significant viral replication. Pretreatment of mice to activate macrophages did not impair dissemination of the virus. Thus, cytomegalovirus can infect a subpopulation of cells enriched in macrophages, and although little replication occurs, such infection facilitates the establishment of persistent infection.

Animals↗
PubMed1980

Comparison of techniques for recovering murine cytomegalovirus from a macrophage-enriched subpopulation of mice.

We previously demonstrated the transmission of murine cytomegalovirus to syngeneic mice and preformed monolayers of mouse embryo fibroblasts with plastic-adherent peritoneal exudate cells from infected mice as a source of macrophages. In the present studies we compared this standard feeder layer method with a reverse feeder layer method in which the adhering peritoneal exudate cells remained attached to plastic and to which were added mouse embryo fibroblasts. Recovery of virus from the adherent peritoneal exudate cells of infected mice was achieved with both methods. Whereas the standard method achieved greater accuracy and usually recovered more virus, the reverse method appeared to recover virus more frequently and required fewer cells to perform the assay. Furthermore, the reverse method demonstrated the survival of murine cytomegalovirus in adhering cells after culture periods of up to 2 weeks.

Animals↗
PubMed1979

Enhanced immune response late in primary cytomegalovirus infection of mice.

Murine cytomegalovirus (MCMV) infection has been previously shown to depress humoral and cell-mediated functions to non-MCMV antigens. In this report we show that in C3D2 mice undergoing nonlethal primary infection the depressed anti-sheep RBC plaque-forming cell (PFC) response is followed by an enhanced PFC response. Infected mice often generated twice the number of PFC per spleen than that of control mice. Total numbers of spleen cells as well as the recovery of virus from spleens of infected mice did not distinguish the depressed from the enhanced phase of the response. Investigation of the kinetics of the response revealed a defect in shutdown regulation. This enhanced PFC response during primary MCMV infection was not reflected in measurements of serum hemagglutinin. These findings suggest that MCMV induces an impairment of immunoregulation.

Animals↗
PubMed1977

Progressive inhibition of T-cell function preceding clinical signs of cytomegalovirus infection in mice.

Groups of mice that received a predominantly lethal or a nonlethal dose of murine cytomegalovirus (CMV) were studied prospectively to correlate clinical observations with detection of virus in spleen cells and with the response of spleen cells to the thymus-derived (T-) cell mitogen concanavalin A (con A). In both groups of mice, virus was virtually cleared from spleen cells by day 8 after infection. Depression of the spleen cell response to con A preceded clinical signs of infection, was more severe in the lethally infected group, and improved as clinical signs cleared in the few surviving mice. Serum from infected mice depressed the response of uninfected spleen cells to con A. These findings support the hypothesis that clinical illness and death from CMV infection of mice are a consequence of events that follow the depression of T-cell function by CMV. This depression is at least partially mediated by a humoral mechanism.

Animals↗