Inflammatory pseudotumor of the liver. Evidence for follicular dendritic reticulum cell proliferation associated with clonal Epstein-Barr virus

Am J Surg Pathol. 1996 Jun;20(6):747-53. doi: 10.1097/00000478-199606000-00013.

Abstract

We describe an "inflammatory pseudotumor" of the liver that, which on detailed investigation, proved that the spindle-cell component of this lesion is derived from follicular dendritic reticulum cells (FDRC). This contention is supported by morphologic observations and by immunophenotype. The FDRC population contain Epstein-Barr virus (EBV). It is known that FDRC express the EBV receptor CD21. In this particular case, the FDRC contained clonal EBV genomes, EBV RNA (EBER) transcripts, and expressed EBV latent membrane protein (LMP1). DNA sequencing of PCR products showed three point mutations compared with the standard LMP1 sequence of the EBV strain B95-8. The findings in this case corroborate those of other investigators concerning the possible role of EBV in the development of some inflammatory pseudotumors, including the recent production of functionally active EBV-transformed FDRC-like cell lines. This association could prove instructive in delineating the histogenesis of these tumors and further assist in making prognostic and therapeutic decisions.

Publication types

  • Case Reports
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Base Sequence
  • Biopsy, Needle
  • Blotting, Southern
  • Cell Division
  • Dendritic Cells / pathology
  • Female
  • Herpesviridae Infections / immunology
  • Herpesviridae Infections / pathology*
  • Herpesvirus 4, Human / isolation & purification*
  • Humans
  • Immunohistochemistry
  • Immunophenotyping
  • Ki-67 Antigen
  • Liver Neoplasms / immunology
  • Liver Neoplasms / pathology*
  • Liver Neoplasms / virology*
  • Molecular Sequence Data
  • Neoplasm Proteins / analysis
  • Nuclear Proteins / analysis
  • RNA, Viral / analysis
  • Receptors, Complement 3d / analysis
  • Tumor Virus Infections / immunology
  • Tumor Virus Infections / pathology*

Substances

  • Ki-67 Antigen
  • Neoplasm Proteins
  • Nuclear Proteins
  • RNA, Viral
  • Receptors, Complement 3d