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BLV-infected lymphocytes exhibit two patterns of expression as determined by Ig and CD5 markers

R Meirom1, J Brenner, Z Trainin

  • 1Department of Immunology, Kimron Veterinary Institute, Bet Dagan, Israel.

Veterinary Immunology and Immunopathology
|March 1, 1993
PubMed

Insights

Bovine leucosis virus (BLV) infection impacts cow lymphocytes differently. BLV causes B lymphocyte proliferation in some cows, while others show a decrease in lymphocyte numbers and specific cell types.

Area of Science:

  • Veterinary Immunology
  • Virology
  • Cell Biology

Background:

  • Bovine leucosis virus (BLV) is a significant pathogen in cattle.
  • Understanding lymphocyte responses to BLV is crucial for disease management.
  • Persistent lymphocytosis (PL) is a clinical manifestation of BLV infection.

Purpose of the Study:

  • To investigate the differential expression of Ig and CD5 markers on lymphocytes in BLV-infected cows.
  • To compare lymphocyte populations in cows with and without persistent lymphocytosis.
  • To elucidate the impact of BLV on bovine lymphocyte subsets.

Main Methods:

  • Categorization of cows into three groups: BLV seropositive with persistent lymphocytosis (BLV + PL +), BLV seropositive without persistent lymphocytosis (BLV + PL-), and BLV negative.
  • Enumeration of lymphocytes.
  • Double staining immunofluorescence to determine the expression of Ig and CD5 on peripheral blood mononuclear cells (PBMC).

Main Results:

  • Cows with BLV and persistent lymphocytosis exhibited massive proliferation of B lymphocytes expressing both Ig and CD5.
  • Cows with BLV but without persistent lymphocytosis showed a significant decrease in CD5+Ig-, CD5-Ig+, and CD5+Ig+ cells, along with reduced total lymphocyte counts.
  • BLV infection appears to influence lymphocyte populations through distinct pathways.

Conclusions:

  • BLV infection induces divergent effects on bovine lymphocyte populations.
  • The observed differences in lymphocyte response may be linked to the genetic characteristics of the host cells.
  • Further research is warranted to explore the mechanisms underlying these differential pathways.

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