## Abstract Recent studies indicate that a defective proliferative response of HIV‐specific CD8+ T cells is associated with the lack of virologic control in chronic HIV infection in humans. The possible mechanisms that might be responsible for the reduced proliferative potential of HIV‐specific CD8
T cell therapy of human CMV and EBV infection in immunocompromised hosts
✍ Scribed by Stanley R. Riddell; Philip D. Greenberg
- Publisher
- John Wiley and Sons
- Year
- 1997
- Tongue
- English
- Weight
- 142 KB
- Volume
- 7
- Category
- Article
- ISSN
- 1052-9276
No coin nor oath required. For personal study only.
✦ Synopsis
Acute virus infections in normal hosts are typically controlled by the development of a host immune response that includes MHC-restricted virus-specific T cells. Many viruses have developed methods to evade T cell recognition to facilitate initial infection and the establishment of a persistent infection in the host. Human cytomegalovirus (CMV) and Epstein-Barr virus (EBV) are ubiquitous human pathogens that utilise novel strategies to evade immune elimination. Despite these evasion methods, CD4 + and CD8 + T cells expressing T cell receptors have been shown to play a pivotal role in controlling initial infection and in maintaining CMV and EBV in a latent state. However, in settings of iatrogenic or acquired T cell deficiency, primary infection or reactivation of CMV and EBV frequently progresses to cause life threatening disease. In this article the role of MHC-restricted CD8 + and CD4 + T cell responses in controlling CMV and EBV infections in healthy individuals and the development of novel strategies to restore protective T cell immunity to deficient hosts by the adoptive transfer of virus-specific T cells is reviewed. 1997 by
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