Janice L. Beland

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Intranasal Herpes simplex virus type 1 (HSV-1) infection of mice caused pneumonia. Manifestations of the disease included: histological pneumonitis, pulmonary influx of lymphocytes, decreased pulmonary compliance, and decreased survival. Immunohistochemical staining demonstrated iNOS induction and the nitrotyrosine antigen in the lungs of infected, but not(More)
We studied the susceptibility of B cell-deficient mice to encephalomyelitis following intraperitoneal inoculation of HSV-1. B cell-deficient mice developed striking CNS signs including tail atony, clumsy gait and limb paralysis after HSV-1 infection. In addition, B cell-deficient mice had decreased survival (LD50 = 2.2 x 10(7) PFU) compared to control(More)
The importance of natural killer (NK) cells in the resistance to herpes simplex virus type 1 (HSV-1), a common infection of immunocompromised patients, is unclear. Previous data on the role of NK cells in murine HSV-1 infection has been contradictory. Adoptive transfer studies suggested that NK cells mediated resistance to HSV-1, but in vivo depletion(More)
To gain further insights in the pathogenesis of herpesvirus pneumonia in allogeneic bone marrow transplant recipients, transplanted mice (B10.BR --> CBA) with graft-versus-host disease (GVHD) and control mice (transplanted mice without GVHD and normal CBA mice) were infected intranasally with herpes simplex virus type 1 (HSV-1). When compared with infected(More)
Posttransplant infection associated with host immune deficiency is the major cause of nonrelapse mortality of human bone marrow transplant recipients. In a new murine model of posttransplant infection, allogeneic bone marrow transplant recipients were infected with herpes simplex virus-1 (HSV-1) via intraperitoneal inoculation 12 weeks after(More)
All T cells of TCR-beta transgenic mice bear a single TCR-beta chain and consequently the diversity of the TCR may be reduced by as much as one million-fold. Despite this limited diversity, many measures of lymphocyte function in these mice are normal. We have previously demonstrated that lymphoid cells from TCR-beta mice are unable to mediate an intense(More)
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