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Epstein-Barr virus recombinants with specifically mutated BCRF1 genes
S Swaminathan1, R Hesselton, J Sullivan
1Dorrance H. Hamilton Research Laboratories, Department of Medicine, Jefferson Medical College, Thomas Jefferson University, Philadelphia, Pennsylvania 19107-6799.
Journal of Virology
|December 1, 1993
Summary
Mutating the Epstein-Barr virus (EBV) BCRF1 gene did not affect infection or cell growth. However, it impaired the virus's ability to block host immune responses.
Area of Science:
- Virology
- Immunology
- Molecular Biology
Background:
- Epstein-Barr virus (EBV) establishes lifelong infections in humans.
- The BCRF1 gene product of EBV is implicated in viral pathogenesis.
- Understanding BCRF1's role is crucial for controlling EBV-associated diseases.
Purpose of the Study:
- To investigate the function of the Epstein-Barr virus (EBV) BCRF1 gene.
- To determine BCRF1's role in latent infection, B-lymphocyte transformation, and host immune modulation.
Main Methods:
- Construction of EBV recombinants with mutated or deleted BCRF1 genes.
- Infection of primary human B lymphocytes to assess latent infection and growth transformation.
- Tumorigenicity assays in SCID mice.
- Assay for blocking gamma interferon release in infected cell cultures.
Main Results:
- Mutating or deleting the BCRF1 gene had no impact on EBV's ability to initiate/maintain latent infection, transform B cells into lymphoblastoid cell lines (LCLs), or replicate.
- BCRF1 mutants did not affect LCL tumorigenicity in SCID mice.
- Mutant BCRF1-infected cells failed to block gamma interferon release, unlike wild-type EBV.
Conclusions:
- The BCRF1 gene is not essential for EBV's lytic replication, latent infection, or B-cell transformation.
- BCRF1 plays a significant role in modulating host immune responses, specifically by blocking gamma interferon release.
- This study establishes the first functional assay for BCRF1 expression and highlights its importance in EBV-host interactions.