期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：1999
卷号：96
期号：16
页码：9281-9286
DOI：10.1073/pnas.96.16.9281
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：To determine whether established CD8+ T cell memory to an epitope prominent during the replicative phase of a {gamma}-herpesvirus infection protects against subsequent challenge, mice were primed with a recombinant vaccinia virus expressing the p56 peptide and then boosted by intranasal exposure to an influenza A virus incorporating p56 in the neuraminidase protein. Clonally expanded populations of functional, p56-specific CD8+ T cells were present at high frequency in both the lung and the lymphoid tissue 1 month later, immediately before respiratory challenge with {gamma}HV-68. This prime-and-boost regime led to a massive reduction of productive {gamma}HV-68 infection in the respiratory tract and, initially, to much lower levels of latency in both the regional lymph nodes and the spleen. The CD8+ T cell response to another epitope (p79) was diminished, there was less evidence of B cell activation, and the onset of the CD4+ T cell-dependent splenomegaly was delayed. Within 3-4 weeks of the {gamma}HV-68 challenge, however, the extent of latent infection in the lymph nodes and spleen was equivalent, and both groups developed the prominent infectious mononucleosis-like syndrome that is characteristic of this infection. The reverse protocol (influenza then vaccinia) seemed to be slightly less effective. Even though immune CD8+ T cells may be present at the time and site of virus challenge, establishing a high level of CD8+ T cell memory to lytic-phase epitopes alone does not protect against the longer-term consequences of this {gamma}HV infection.
