In the absence of T cells, natural killer cells protect from mortality due to HSV-1 encephalitis.

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 approaches demonstrated that NK cells were not important.

B cell-deficient mice have increased susceptibility to HSV-1 encephalomyelitis and mortality.

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.

Recombinant CD40L treatment protects allogeneic murine bone marrow transplant recipients from death caused by herpes simplex virus-1 infection.

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 transplantation. Allogeneic transplant recipients with graft-versus-host disease (GVHD) had significantly increased mortality from HSV-1 encephalitis, with deficiencies of both specific anti-HSV-1 antibody and total serum IgG2a.

A role for transforming growth factor-beta1 in the increased pneumonitis in murine allogeneic bone marrow transplant recipients with graft-versus-host disease after pulmonary herpes simplex virus type 1 infection.

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 control mice, infected allogeneic transplant recipients with GVHD showed increased periluminal mononuclear cell infiltrates.

Suppression of herpes simplex virus type 1 (HSV-1)-induced pneumonia in mice by inhibition of inducible nitric oxide synthase (iNOS, NOS2).

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 uninfected mice, suggesting that nitric oxide contributes to the development of pneumonia.