Interaction between Epstein-Barr virus and a T cell line (HSB-2) via a receptor phenotypically distinct from...

Area of Science:

• Immunology
• Virology
• Cell Biology

Background:

• Epstein-Barr virus (EBV) causes mononucleosis and cancers.
• EBV typically infects cells via complement receptor type 2 (CR2, CD21), found on B lymphocytes and other cells.
• The mechanism of EBV entry into T lymphocytes remains incompletely understood.

Purpose of the Study:

• To identify and characterize the receptor used by EBV for entry into T lymphocytes.
• To determine if T cells utilize CR2 for EBV infection.
• To investigate the molecular nature of the EBV receptor on T cells.

Main Methods:

• Utilized leukemic T cell line HSB-2, lacking CR2 expression.
• Employed biotin-conjugated EBV for binding assays and blocking experiments with anti-EBV antibodies and C3.
• Assessed CR2 mRNA absence via Northern blotting and PCR.
• Confirmed viral internalization and infection using electron microscopy, Southern blotting for EBV-DNA, and PCR for EBNA-1 transcripts.
• Investigated CR2 cDNA homology in HSB-2 transcripts under low stringency hybridization.

Main Results:

• HSB-2 cells, negative for CR2, demonstrated specific binding to EBV.
• Aggregated C3 also bound HSB-2 and partially inhibited EBV binding.
• HSB-2 cells showed viral internalization, EBV-DNA, and EBNA-1 transcripts, indicating successful infection.
• HSB-2 cells expressed a 5.2 kb mRNA transcript with partial homology to the N-terminal half of CR2 cDNA, distinct from B cell CR2 mRNA.
• This transcript lacked homology to the C-terminal half of CR2 cDNA.

Conclusions:

• EBV utilizes a novel receptor on T lymphocytes that is phenotypically distinct from CR2.
• This receptor shares some homology with CR2, particularly in the N-terminal region containing EBV-binding epitopes.
• The findings reveal a new mechanism for EBV tropism towards T lymphocytes, with implications for understanding EBV-associated diseases.