Therefore, an HBL-5 phenotype with expression of CD54 and LMP tends toward an LCL phenotype, and the augmentation of CD54 on the HBL-5 cells in comparison with primary lymphoma cells is likely to be upregulated by LMP, probably resulting from the EBV infection.
Therefore, an HBL-5 phenotype with expression of CD54 and LMP tends toward an LCL phenotype, and the augmentation of CD54 on the HBL-5 cells in comparison with primary lymphoma cells is likely to be upregulated by LMP, probably resulting from the EBV infection.
This study confirms the relatively low frequency of EBV infection in systemic AIDS-NHL in general, but reinforces the notion that EBV may be required for the pathogenesis of AIDS-LC-IBP, as recently suggested by the high frequency of EBV positivity in primary CNS AIDS-NHL which are mostly represented by LC-IBP (2).
We conclude that some AIDS-related lymphomas are associated with eosinophilia and that the eosinophilia may be related to EBV infection and transcriptional activation of the IL-5 gene.
The recent use of DNA restriction fragment length polymorphism (RFLP) probes in linkage with the XLP gene now permit detection of affected males prior to primary EBV infection.
We summarized recent research findings and technological advances that permit accurate diagnosis of carrier females and detection of males with the XLP gene before Epstein-Barr virus infection.
We show that EBV termini are uniformly clonal in sBL, eBL, and AIDS-NHL, strongly suggesting that EBV infection has preceded and, thus, most likely contributed to clonal expansion in these malignancies.
Nuclear protein-2 (EBNA-2) and EBNA-leader protein (-LP) were detected by 12 hr, and by 32 hr were at the levels of stable EBV infection in lymphoblastoid cell lines (LCLs).
Similar to endemic and sporadic Burkitt's lymphoma, monoclonal B-lymphoma subsets were found to be infected with Epstein-Barr virus (EBV) or have c-myc gene rearrangements, suggesting a role for EBV infection or chromosomal translocation in a subset of AIDS NHLs.
In order to assess the generality of a role for the c-fgr gene in the response of B-lymphocytes to EBV-infection, which is controversial, we have analysed c-fgr expression in 6 freshly immortalized cell lines established by EBV (B95-8) infection of B-lymphocytes from the peripheral blood of normal adults and of adults with rheumatoid arthritis, from cord blood, and from foetal liver.
Humans with serologic evidence of Epstein-Barr virus infection had serum antibodies to gp110 and peripheral blood T cells that recognized peptides from gp110 and HLA-Dw4 encompassing the QKRAA determinant.
Humans with serologic evidence of Epstein-Barr virus infection had serum antibodies to gp110 and peripheral blood T cells that recognized peptides from gp110 and HLA-Dw4 encompassing the QKRAA determinant.
It is proposed that during EBV infection, there are multiple copies of the EBERs available to bind to the La ribonucleoprotein and when infection occurs in subjects who have an impaired T cell-mediated response to EBV, and who are genetically predisposed to autoimmunity, there is loss of immunological tolerance to La with production of anti-La (SS-B).
These studies suggest that both the deregulation of MYC transcription and the chromosomal rearrangement in the region of the MYC locus in this B-cell line may have occurred as a result of EBV infection.
In experimental B-cell infections, Epstein-Barr virus induced sustained expression of V(D)J recombinase-activating genes RAG1 and RAG2, whose aberrant activity has been implicated in chromosomal translocations in B-cell neoplasms.
In experimental B-cell infections, Epstein-Barr virus induced sustained expression of V(D)J recombinase-activating genes RAG1 and RAG2, whose aberrant activity has been implicated in chromosomal translocations in B-cell neoplasms.
Although earlier studies of AIDs burkitt's lymphoma cell lines suggested that IL-10 expression required EBV infection, 7 of 12 AIDS LCLs that expressed IL-10 did so in the absence of EBV by EBER in situ hybridization.
Transient stimulation of quiescent B lymphocytes with either a cocktail of anti-CD40, anti-IgM, and IL4, or EBV results in the rapid expression of the same four genes, suggesting that, after infection, EBV exploits the normal program of B-lymphocyte cell cycle activation.
These studies suggest that (1) alternative splicing of CD44 isoforms is differentially regulated depending on the mode and state of cell activation, and that (2) the CD44 V6/V7 isoforms may represent B-cell activation antigens that are induced by mitogenic stimulation but not following EBV infection.
EBV infection was detected with in situ hybridization for EBV-encoded RNAs (EBERs) and by immunohistochemical staining for latent membrane protein 1 (LMP-1).
Although molecular events in the neoplastic transformation of B-cells are not well understood, Epstein-Barr virus infection and bcl-2 protein overexpression have been postulated to have etiologic roles in some lymphomas.