EBV P18 Mosaic protein (DAG1582)

EBV P18 Mosaic protein, recombinant protein from E. coli

Product Overview
Recombinant EBV p18 protein was expressed in E. coli and purified by proprietary chromatographic technique.
> 95% pure as determined by 10% PAGE (coomassie staining).
50mM Tris-Hcl pH 8.0, 60mM NaCl, 10mM glutathione and 50% glycerol.
2-8°C short term, -20°C long term
The Epstein-Barr virus (EBV), also called Human herpes virus 4 (HHV-4), is a virusof the herpes family(which includes Herpes simplex virusand Cytomegalovirus. On infecting the B-lymphocyte, the linear virus genome circularizes and the virus subsequently persists within the cell as an episome. The virus can execute several distinct programs of gene expressionwhich can be broadly categorized as being lytic cycle or latent cycle. The lytic cycleor productive infection results in staged expression of a host of viral proteinswith the ultimate objective of producing infectious virions. Formally, this phase of infection does not inevitably lead to lysis of the host cellas EBV virions are produced by budding from the infected cell. The latent cycle(lysogenic) programs are those that do not result in production of virions. A very limited, distinct set of viral proteins are produced during latent cycle infection. These include Epstein-Barr nuclear antigen(EBNA)-1, EBNA-2, EBNA-3A, EBNA-3B, EBNA-3C, EBNA-leader protein (EBNA-LP) and latent membrane proteins(LMP)-1, LMP-2A and LMP-2B and the Epstein-Barr encoded RNAs(EBERs).
Epstein–Barr virus; Herpesviridae; Gammaherpesvirinae; Lymphocryptovirus; Human herpesvirus 4; HHV-4; EBV; p18 protein; Epstein-Barr Virus (EBV) p18 (VP26); Recombinant EBV (HHV-4) p18 virus capsid antigen (VP26, BFRF3); VP26; BFRF3; EBV p18; Epstein–Barr


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Increased antibody levels to stage-specific Epstein-Barr virus antigens in systemic autoimmune diseases reveal a common pathology


Authors: Sternbaek, Louise; Draborg, Anette H.; Osterlund, Mark T.; Iversen, Line V.; Troelsen, Lone; Theander, Elke; Nielsen, Christoffer T.; Jacobsen, Soren; Houen, Gunnar

The immune responses to antigens from different stages of the Epstein-Barr virus (EBV) life cycle were investigated in systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), Sjogren's syndrome (SS), and systemic sclerosis (SSc) to gain knowledge of EBV's involvement in the etiology of systemic autoimmune diseases (SADs) and for an overview of the humoral immune responses against EBV. Investigations were performed by the use of ELISA. IgM, IgA, and IgG antibody binding to 11 EBV antigens: EBNA1, EBNA2, BALF5, EAD, BALF2, EA/R, VCA p18, VCA p23, gB, gp350, and gp42 were examined in serum pools from SAD patients and healthy controls (HCs). Increased antibody levels against the 11 EBV antigens in the SAD pools were seen compared to the HC pool. Specifically, SLE was characterized by strongly increased IgA to EAD both compared to HCs and other SADs, and RA was characterized by increased IgM levels to several EBV antigens. The SADs may be partly distinguished by their differential immune responses to various antigens in the EBV life cycle. All together, these findings support an association between EBV infection and SADs.

Aberrant Epstein-Barr virus persistence in HIV carriers is characterized by anti-Epstein-Barr virus IgA and high cellular viral loads with restricted transcription


Authors: Stevens, Servi J. C.; Smits, Paul H. M.; Verkuijlen, Sandra A. W. M.; Rockx, Davy A. P.; van Gorp, Eric C. M.; Mulder, Jan W.; Middeldorp, Jaap M.

Objective: Epstein-Barr virus (EBV)-positive lymphomas in HIV carriers are paralleled by elevated EBV-DNA loads in the circulation. Approximately 20% of asymptomatic HIV carriers also show elevated circulating EBV-DNA loads. We aimed to characterize the nature of this EBV DNA and to determine the transcriptional phenotype of EBV in blood, in relation to serological parameters. Design: A total of 197 random asymptomatic HIV carriers, representing 2% of the Dutch HIV-positive population, were sampled for blood, peripheral blood mononuclear cells and plasma. in addition, 39 EBV-DNA carriers were sampled twice, with a 5-year interval. Methods: EBV-DNA loads were determined by LightCycler-based real-time polymerase chain reaction (PCR). EBV transcription was studied by nucleic acid sequence-based amplification and reverse transcriptase PCR. IgA and IgG antibodies to EBV antigens EBNA1 and VCA-p18 were quantified by synthetic peptide-based enzyme-linked immunosorbent assay. Results: Elevated EBV-DNA loads were found in whole blood of 19.3% of the tested HIV population, which were persistent in 82%. Plasma samples were EBV-DNA negative and circulating EBV DNA could be attributed to the B-cell compartment. Transcription of only LMP2 and (non-translated) transcripts from the BamHI-A region of the EBV genome was found, whereas EBNA1, LMP1 and lytic EBV transcripts were absent despite high cellular EBV-DNA loads. IgA-reactivity to VCA-p18 was seen in 69%. IgG to VCA-p18 was significantly higher in high EBV-DNA load carriers. Conclusion: Asymptomatic HIV carriers show aberrant EBV persistence in the circulation, characterized by elevated, B-cell-associated EBV-DNA loads. EBV transcription is restricted, arguing for EBV gene shutdown in circulating EBV-carrying B cells. Increased IgA and IgG reactive to VCA-p18 is indicative of increased lytic EBV replication, possibly occurring at mucosal lymphoid sites but not in the circulation. (C) 2007 Wolters Kluwer Health | Lippincott Williams & Wilkins.

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