Consistent transcription of the Epstein-Barr virus LMP2 gene in nasopharyngeal carcinoma

Abstract

Two species of the Epstein-Barr virus-encoded latent membrane protein 2, LMP2A and LMP2B, are generated by alternative splicing, each species having a distinct first exon. LMP2 transcription in undifferentiated nasopharyngeal carcinoma (NPC), which is consistently associated with the Epstein-Barr virus, was investigated. Fifteen NPC specimens were analyzed by Northern (RNA) blot and RNA-based polymerase chain reaction; the LMP2A transcript was present in all specimens except one. In some specimens the LMP2B transcript was also detected. Sequence analysis of LMP2 cDNAs obtained from two NPC specimens revealed four mutations in exon 1 of the LMP2A transcript, which were present in both tumors and which resulted in nonconservative amino acid changes. These data suggest that the LMP2 expressed in NPC is distinct from that which is expressed in lymphoid cells.

Analysis of epstein‐barr virus infection in nasopharyngeal biopsies from a group at high risk of nasopharyngeal carcinoma

“…Analysis of undifferentiated NPC, and more recent studies on receptor-positive epithelial cells exposed to the virus in vitro, have identified a number of viral markers characteristic of non-productive infection in an epithelial environment. These are expression of the small non-polyadenylated nuclear RNAs (EBERs), of the spliced rightward-running BamHI A RNAs, and of a BamHI F promoter-driven EBNAl mRNA with a unique BamHI FQ/U/K splice structure (Wu et al, 1991;Brooks et al, 1992;Busson et al, 1992;Gilligan et al, 1991;Li et aL, 1992;Niedobitek et al, 1992). The EBERs are by far the most abundant latency-associated transcripts and are readily detectable by in situ hybridization (Wu ef al., 1991;Niedobitek et al, 1992) whilst the other less abundant RNAs are detectable by polymerase chain reaction-mediated cDNA amplification across splice junctions (Brooks ef al., 1992).…”

Comparison of Humoral Immune Responses to Epstein-Barr Virus and Kaposi’s Sarcoma–Associated Herpesvirus Using a Viral Proteome Microarray

“…However, EBV can be routinely detected in circulating latently infected B cells of healthy seropositive individuals, whereas detection of KSHV in blood is rare [44][45][46]. The preferential ability to detect serum IgA responses against EBV vs KSHV on the protein arrays may also be related to in vivo infection of mucosal epithelial cells by EBV because the most frequently observed antigens were latency proteins or lytic replicative proteins known to be expressed in epithelial cells [47][48][49][50]. KSHV infects endothelial cells as well as B cells, but the contribution of endothelial cells to in vivo viral persistence is not well understood.…”

Tonic B‐cell and viral ITAM signaling: context is everything

“…(C) Cells from the peritoneal cavity of wildtype C57/Bl6 and mMT recipient mice were stained for B220 and CD5 to detect B1 B cells. (111,112) and elevated titers of antibodies to LMP2A found in 64% of NPC patients (113). The inability of LMP2A to transform human foreskin kerotinocytes and the absence of tumor formation in transgenic mice suggest that LMP2A itself is not oncogenic (114,115).…”