Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0021345 (infectious mononucleosis)
 3,358 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Epstein-Barr virus (EBV) is a member of the human herpesvirus family and, like many other herpesviruses, maintains a lifelong latent association with B lymphocytes and a permissive association with stratified epithelium in the oropharynx. Clinical manifestations of primary EBV infection range from acute infectious mononucleosis to an asymptomatic persistent infection. EBV is also associated with a number of malignancies in humans. This review discusses features of the biology of the virus, both in cell culture systems and in the natural host, before turning to the role of the immune system in controlling EBV infection in healthy individuals and in individuals with EBV-associated diseases. Cytotoxic T cells that recognize virally determined epitopes on infected cells make up the major effector arm and control the persistent infection. In contrast, the options for immune control of EBV-associated malignancies are more restricted. Not only is antigen expression restricted to a single nuclear antigen, EBNA1, but also these tumor cells are unable to process EBV latent antigens, presumably because of a transcriptional defect in antigen-processing genes (such as TAP1 and TAP2). The likelihood of producing a vaccine capable of controlling the acute viral infection and EBV-associated malignancies is also discussed.
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PMID:Immune regulation in Epstein-Barr virus-associated diseases. 756 11

Like EBV-infected humans with infectious mononucleosis, mice infected with the rodent gammaherpesvirus MHV-68 develop a profound increase in the number of CD8+ T cells in the circulation. In the mouse model, this lymphocytosis consists of highly activated CD8+ T cells strikingly biased toward V beta 4 TCR expression. Moreover, this expansion of V beta 4+CD8+ T cells does not depend on the MHC haplotype of the infected animal. Using a panel of lacZ-inducible T cell hybridomas, we have detected V beta 4-specific T cell stimulatory activity in the spleens of MHV-68-infected mice. We show that the appearance and quantity of this activity correlate with the establishment and magnitude of latent viral infection. Furthermore, on the basis of Ab blocking studies as well as experiments with MHC class II, beta2-microglobulin (beta2m) and TAP1 knockout mice, the V beta 4-specific T cell stimulatory activity does not appear to depend on conventional presentation by classical MHC class I or class II molecules. Taken together, the data indicate that during latent infection, MHV-68 may express a T cell ligand that differs fundamentally from both conventional peptide Ags and classical viral superantigens.
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PMID:Apparent MHC-independent stimulation of CD8+ T cells in vivo during latent murine gammaherpesvirus infection. 1041 50