Epstein±Barr nuclear antigen 1, or EBNA-1, is required for the replication of the EBV genome as an extrachromosomal element and is a key transcriptional regulator of this virus's latent gene expression. In this review we will describe the salient features of EBNA-1 and oriP, the latent origin of EBV
Epstein–Barr virus latent infection in vivo
✍ Scribed by Neil M. Steven
- Publisher
- John Wiley and Sons
- Year
- 1997
- Tongue
- English
- Weight
- 279 KB
- Volume
- 7
- Category
- Article
- ISSN
- 1052-9276
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✦ Synopsis
Epstein-Barr virus (EBV) is an exclusively human herpes virus which is recognised as the causative agent of infectious mononucleosis and which is implicated in the aetiology of several cancers. However, it is particularly remarkable that this virus is harboured without causing symptoms for the lifetime of most immunocompetent adults. Virus and host have co-evolved over millions of years, achieving a balance between viral persistence and immune control. It is this dynamic equilibrium which is the focus of this review. The main site of viral persistence is within latently infected lymphocytes, although infectious virus is also released into saliva from productively infected cells in the oropharynx. In vitro, EBV efficiently transforms resting B cells to activated, perpetually dividing lymphoblasts. These express a repertoire of eight viral antigens, several of which have been found to be targets for cytotoxic T cell (CTL) responses in healthy carriers. Transformed lymphoblasts are susceptible to immune control in vivo, and are abundant only during primary infection or in individuals with impaired cell mediated immunity. Other types of viral latent infection have been identified in malignant cell lines, in which EBV expresses a more restricted range of antigens. These also may have their in vivo equivalents during natural infection in healthy carriers. It is likely that the virus evades elimination by the immune system by establishing infection in non-activated, relatively non immunogenic B cells, in which the main CTL target antigens are not expressed. 1997 by John Wiley & Sons, Ltd.
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