| Pathology and Pathogenesis Immunohistochemistry
analysis has shown that viral antigens are distributed primarily within the endothelium of
capillaries throughout various tissues from patients with HPS. Marked accumulations of
hantaviral antigens are seen in the pulmonary microvasculature and in follicular dendritic
cells within the lymphoid follicles of spleen and lymph nodes. Hantaviral nucleic acids
can also be localized to endothelial and inflammatory cells in tissues from HPS cases by
using in situ hybridization. Electron micrographic studies confirm the infection of
endothelial cells and macrophages in the lungs of HPS patients. Typical hantaviral
inclusions are seen frequently in pulmonary endothelial cells, and their identity can be
confirmed by immunolabeling. In the heart, endothelial staining is mainly in the
capillaries of the myocardium and varies from focal immunostaining in some cases to
diffuse and extensive staining in others. Occasionally, staining of endothelial cells
lining the endocardium is observed.
Functional impairment of vascular endothelium is central to the pathogenesis of HPS.
However, the pathogenesis of HPS is complex, and a myocardial depressant may contribute
significantly to the mortality of this disease. It is unclear how the shock syndrome
relates to factors such as viral distribution and immunologic and pharmacological
mediators of capillary permeability. There appears to be compartmentalization of a
selective immune response in the lungs of HPS patients in combination with extremely high
levels of viral antigens in the pulmonary vasculature. This feature suggests that the
mechanism of inflammatory cell recruitment in the lungs of HPS patients may result from
specific attraction and adherence of a selective population of inflammatory cells to an
activated pulmonary microvascular endothelium.
|
National
Center for Infectious Diseases
