Lymphocytic choriomeningitis: Ultrastructural pathology

David Walker, Frederick A. Murphy, Sylvia G. Whitfield, Sally P. Bauer

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

The pathogenesis of lymphocytic choriomeningitis (LCM) virus infection was studied in mice by associating the development of ultrastructural changes with parallel light microscopic alterations and the build-up of viral antigen as detected by immunofluorescence. From early in the course of the disease, viral antigen was localized in the choroid plexus and ependymal epithelium and the arachnoid cells of the meninges. Typical LCM virus particles were found enmeshed in the microvillous border of the choroid plexus and ependyma as a result of budding from plasma membranes and entrapment beneath overlying macrophages and epithelial projections. These virus particles and nascent budding particles were considered the target of the terminal cell-mediated immune (CMI) response. Arenavirus inclusions were observed in the cytoplasm of the same epithelia throughout the late stages of infection, but such antigen masses were effectively sequestered. On the day before death (day 6 postinoculation), mononuclear cells invaded the choroid plexus by extravasation through the central capillary endothelium and basement lamina, and then via emperipolesis and intercellular migration through the epithelium into the cerebrospinal fluid of the ventricles. The most common invading cell type was considered a medium or large lymphocyte, but monocytes and macrophages were also present. Similar cell types invaded the ependyma and the subarachnoid space of the meninges. No cytopathology was associated with the viral infection of the choroid plexus, ependyma, or meninges, nor with the mononuclear cell influx of the CMI reaction to infection. The parenchyma of the brain remained normal throughout infection; there was no evidence of infection, inflammation, or edema. Because correspondence of the immunopathologic target site and the anatomic location of the blood-cerebrospinal fluid barrier occurred only in the choroid plexus, this organ was considered to have the central role in LCM pathogenesis. Its functional breakdown must be the proximate cause of the convulsive diatheses characteristic of the disease.

Original languageEnglish (US)
Pages (from-to)245-265
Number of pages21
JournalExperimental and Molecular Pathology
Volume23
Issue number2
DOIs
StatePublished - 1975
Externally publishedYes

Fingerprint

Lymphocytic Choriomeningitis
Pathology
Viruses
Cerebrospinal fluid
Choroid Plexus
Viral Antigens
Macrophages
Ependyma
Meninges
Antigen-antibody reactions
Lymphocytes
Lymphocytic choriomeningitis virus
Cell membranes
Epithelium
Virus Diseases
Infection
Brain
Virion
Blood
Cerebrospinal Fluid

ASJC Scopus subject areas

  • Clinical Biochemistry
  • Molecular Biology
  • Pathology and Forensic Medicine

Cite this

Lymphocytic choriomeningitis : Ultrastructural pathology. / Walker, David; Murphy, Frederick A.; Whitfield, Sylvia G.; Bauer, Sally P.

In: Experimental and Molecular Pathology, Vol. 23, No. 2, 1975, p. 245-265.

Research output: Contribution to journalArticle

Walker, David ; Murphy, Frederick A. ; Whitfield, Sylvia G. ; Bauer, Sally P. / Lymphocytic choriomeningitis : Ultrastructural pathology. In: Experimental and Molecular Pathology. 1975 ; Vol. 23, No. 2. pp. 245-265.
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