| pubmed-article:18996483 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18996483 | lifeskim:mentions | umls-concept:C0014644 | lld:lifeskim |
| pubmed-article:18996483 | lifeskim:mentions | umls-concept:C0006826 | lld:lifeskim |
| pubmed-article:18996483 | lifeskim:mentions | umls-concept:C0332281 | lld:lifeskim |
| pubmed-article:18996483 | lifeskim:mentions | umls-concept:C0439662 | lld:lifeskim |
| pubmed-article:18996483 | lifeskim:mentions | umls-concept:C0870509 | lld:lifeskim |
| pubmed-article:18996483 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:18996483 | pubmed:dateCreated | 2008-12-5 | lld:pubmed |
| pubmed-article:18996483 | pubmed:abstractText | Persistent Epstein-Barr virus (EBV) infection remains asymptomatic in the majority of virus carriers, despite the potent growth transforming potential of this virus. The increased frequency of EBV associated B cell lymphomas in immune compromised individuals suggests that tumor-free chronic infection with this virus is in part due to immune control. Here we discuss the evidence that loss of selective components of EBV specific immunity might contribute to EBV associated malignancies, like nasopharyngeal carcinoma, Burkitt's and Hodgkin's lymphoma, in otherwise immune competent patients. Furthermore, we discuss how current vaccine approaches against EBV might be able to target these selective deficiencies. | lld:pubmed |
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