Regulated expression of galectin-1 after in vitro productive infection with herpes simplex virus type 1: implications for T cell apoptosis

Int J Immunopathol Pharmacol. 2005 Oct-Dec;18(4):615-23. doi: 10.1177/039463200501800402.


Apoptosis of cytotoxic T lymphocytes by herpes simplex virus type-1 (HSV-1) has been reported to be a relevant mechanism of viral immune evasion. Galectin-1 (Gal-1), an endogenous lectin involved in T-cell apoptosis, has recently gained considerable attention as a novel mechanism of tumor-immune evasion. Here we investigated whether infection of cells with HSV-1 can modulate the expression of Gal-1. Results show that pro-apoptotic Gal-1, but not Gal-3, is remarkably up-regulated in cell cultures infected with HSV-1. In addition, this protein is secreted to the extracellular milieu, where it contributes to apoptosis of activated T cells in a carbohydrate-dependent manner. Since many viruses have evolved mechanisms to counteract the antiviral response raised by the infected host, our results suggest that HSV-1 may use galectin-1 as a weapon to kill activated T cells and evade specific immune responses.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / physiology*
  • Blotting, Western
  • Chlorocebus aethiops
  • Electrophoresis, Polyacrylamide Gel
  • Epithelial Cells / pathology
  • Fluorescent Antibody Technique, Indirect
  • Galectin 1 / biosynthesis*
  • Galectin 1 / genetics
  • Galectin 3 / genetics
  • Galectin 3 / physiology
  • Gene Expression Regulation / physiology*
  • Herpes Simplex / pathology*
  • Herpesvirus 1, Human*
  • Humans
  • Immune Tolerance
  • T-Lymphocytes / pathology*
  • Vero Cells


  • Galectin 1
  • Galectin 3