ArticleJournal of virology2005
An optimized CD8+ T-cell response controls productive and latent gammaherpesvirus infection.
Article in Journal of virology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 72 citations in OpenAlex.
- CD154:CD11b blockade enhances CD8+ T cell differentiation during infection but not transplantation.JCI insight · 2025Article
- A replication-deficient gammaherpesvirus vaccine protects mice from lytic disease and reduces latency establishment.NPJ vaccines · 2024Article
- T cell-extrinsic IL-1 signaling controls long-term gammaherpesvirus infection by suppressing viral reactivation.Virology · 2022Article
- Article
- T Cell-Intrinsic Interleukin 17 Receptor A Signaling Supports the Establishment of Chronic Murine Gammaherpesvirus 68 Infection.Journal of virology · 2022Article
- T Cell-Intrinsic Interferon Regulatory Factor 1 Expression Suppresses Differentiation of CD4Journal of virology · 2021Article
- Th2 Cytokine Modulates Herpesvirus Reactivation in a Cell Type Specific Manner.Journal of virology · 2021Article
- TCR Transgenic Mice: A Valuable Tool for Studying Viral Immunopathogenesis Mechanisms.International journal of molecular sciences · 2020Review
- Deletion of immune evasion genes provides an effective vaccine design for tumor-associated herpesviruses.NPJ vaccines · 2020Article
- Memory T cell-mediated rejection is mitigated by FcγRIIB expression on CD8American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2020Article
- Interleukin 16 contributes to gammaherpesvirus pathogenesis by inhibiting viral reactivation.PLoS pathogens · 2020Article
- An Unusual MHC Molecule Generates Protective CD8+ T Cell Responses to Chronic Infection.Frontiers in immunology · 2020Article
- LXR Alpha Restricts Gammaherpesvirus Reactivation from Latently Infected Peritoneal Cells.Journal of virology · 2019Article
- Keeping it in check: chronic viral infection and antiviral immunity in the brain.Nature reviews. Neuroscience · 2016Review
- Autophagy Genes Enhance Murine Gammaherpesvirus 68 Reactivation from Latency by Preventing Virus-Induced Systemic Inflammation.Cell host & microbe · 2016Article
- Pathogen Stimulation History Impacts Donor-Specific CD8(+) T Cell Susceptibility to Costimulation/Integrin Blockade-Based Therapy.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2015Article
- ATM facilitates mouse gammaherpesvirus reactivation from myeloid cells during chronic infection.Virology · 2015Article
- Type I interferon signaling enhances CD8+ T cell effector function and differentiation during murine gammaherpesvirus 68 infection.Journal of virology · 2014Article
- Article
- Systemic and local infection routes govern different cellular dissemination pathways during gammaherpesvirus infection in vivo.Journal of virology · 2013Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Strategies to prime CD8(+) T cells against Murine gammaherpesvirus 68 (gammaHV68; MHV68) latency have, to date, resulted in only limited effects. While early forms of latency (<21 days) were significantly reduced, effects were not seen at later times, indicating loss of control by the primed CD8(+) T cells. In the present study, we evaluated CD8(+) T cells in an optimized system, consisting of OTI T-cell-receptor (TCR) transgenic mice, which generate clonal CD8(+) T cells specific for K(b)-SIINFEKL of OVA, and a recombinant gammaHV68 that expresses OVA (gammaHV68.OVA). Our aim was to test whether this optimized system would result in more effective control not only of acute infection but also of later forms of latent infection than was seen with previous strategies. First, we show that OTI CD8(+) T cells effectively controlled acute replication of gammaHV68.OVA in liver, lung, and spleen at 8 and 16 days after infection of OTI/RAG mice, which lack expression of B and CD4(+) T cells. However, we found that, despite eliminating detectable acute replication, the OTI CD8(+) T cells did not prevent the establishment of latency in the OTI/RAG mice. We next evaluated the effectiveness of OTI T cells in OTI/B6 animals, which express B cells--a major site of latency in wild-type mice--and CD4(+) T cells. In OTI/B6 mice OTI CD8(+) T cells not only reduced the frequency of cells that reactivate from latency and the frequency of cells bearing the viral genome at 16 days after infection (similar to what has been reported before) but also were effective at reducing latency at 42 days after infection. Together, these data show that CD8(+) T cells are sufficient, in the absence of B cells and CD4(+) T cells, for effective control of acute replication. The data also demonstrate for the first time that a strong CD8(+) T-cell response can limit long-term latent infection.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.