LMP1 has critical roles in Epstein-Barr virus (EBV)-driven B-cell transformation, and its expression causes fatal lymphoproliferative disease in immunosuppressed mice.
We concluded that LMP1 is the candidate protein in the upregulation of the TNFalpha gene in T cells and is probably responsible for the pathogenesis of HS in EBV-infected T lymphoproliferative disorders.
In order to clarify the viral subtype that may be involved in the incidence of EBV-associated lymphomas, we analyzed the EBNA-2 and LMP-1 gene polymorphisms and mutations in healthy adults and in patients with EBV-associated cutaneous natural killer(NK)/T-cell lymphoproliferative disorders in Japan.
The molecular detection of the oncogenic variants of the LMP-1 gene in a lymph node biopsy as an indicator of the aggressiveness of the EBV-associated lymphoproliferative disease must be considered with caution.
Tumors from six of the patients with post-transplantation lymphoproliferative disease were positive for EBV and expressed LMP1; two samples were EBV-negative.
The aim of this study was to test whether mutations affecting LMP1 gene expression were present in lymphoproliferative disorders, and, if so, whether their presence correlated with the clinical course of the disease.
Six Epstein-Barr virus (EBV)-related lymphoproliferative disorders were investigated to verify whether the EBV strain harbored by neoplastic cells had the same EBNA-2 and latent membrane protein-1 (LMP-1) DNA sequences of the virus carried by normal lymphocytes of the same patients.
LMP-1 deletions associated with certain aggressive lymphoid neoplasms are not required for the genesis of lymphoproliferative disorders in patients with rheumatic disease.