A triple entente: Virus, neurons, and CD8+ T cells maintain HSV-1 latency

@article{Divito2006ATE,
  title={A triple entente: Virus, neurons, and CD8+ T cells maintain HSV-1 latency},
  author={Sherrie Jill Divito and Thomas L. Cherpes and Robert L Hendricks},
  journal={Immunologic Research},
  year={2006},
  volume={36},
  pages={119-126}
}
Herpes simplex virus type 1 (HSV-1) travels by retrograde transport to sensory ganglia where latency is established. Recurrent disease results from virus reactivation and anterograde transport to nerve termini. Prevention of reactivation requires a complex interplay among virus, neuron, and immune response. Study of this tripartite relationship suggests possible interaction, and even communication among these components, that direct an immune response that allows for control of virus while… Expand
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References

SHOWING 1-10 OF 42 REFERENCES
Herpes simplex virus-specific memory CD8+ T cells are selectively activated and retained in latently infected sensory ganglia.
TLDR
It is concluded that CD8(+) T cells provide active surveillance of HSV-1 gene expression in latently infected sensory neurons. Expand
Anti-CD8 impairs clearance of herpes simplex virus from the nervous system: implications for the fate of virally infected neurons
TLDR
It is suggested that CD8+ T cells play an important role in maintaining the integrity of the sensory nervous system during primary infection with HSV, and viral epitopes recognized by CD8- T cells and restricting class I major histocompatibility complex genes are implicated as interacting genetic determinants of neurovirulence. Expand
Cd8+ T Cells Can Block Herpes Simplex Virus Type 1 (HSV-1) Reactivation from Latency in Sensory Neurons
TLDR
It is demonstrated that CD8+ T cells that are present in the TGs at the time of excision can maintain HSV-1 in a latent state in sensory neurons in ex vivo TG cultures, and it is proposed that when the intrinsic capacity of neurons to inhibit HSv-1 reactivation from latency is compromised, production of HSV -1 immediate early and early proteins might activate CD8- T cells aborting virion production. Expand
Restricted herpes simplex virus type 1 gene expression within sensory neurons in the absence of functional B and T lymphocytes.
TLDR
It is reported that trigeminal ganglia of mice with severe combined immunodeficiency contain individual sensory neurons exhibiting restricted viral gene expression characteristic of latency, which indicates that T and B lymphocytes, while important for the recovery from viral infections, are not required for the establishment or maintenance of latency in neurons. Expand
Immune control of HSV-1 latency.
TLDR
Recent exciting findings supporting a role for the host immune system, particularly CD8+ T cells in maintaining HSV-1 in a latent state are detailed. Expand
Gamma Interferon Can Block Herpes Simplex Virus Type 1 Reactivation from Latency, Even in the Presence of Late Gene Expression
TLDR
The results demonstrate that IFN-γ acts on latently infected neurons to inhibit HSV-1 reactivation, which is associated with an inhibition of the expression of the ICP0 gene (required for reactivation) and a blockade of a step that occurs after theexpression of at least some viral structural genes. Expand
Spontaneous molecular reactivation of herpes simplex virus type 1 latency in mice
TLDR
It is concluded that productive cycle viral genes are abundantly expressed in rare neurons of latently infected murine TG and that these events are promptly recognized by an active local immune response. Expand
Gamma interferon expression during acute and latent nervous system infection by herpes simplex virus type 1
TLDR
It is hypothesized that the persistence of T cells and the sustained IFN-gamma expression occur in response to an HSV-1 antigen in the nervous system and that prolonged secretion of IFN -gamma during latency may modulate a reactivated HSV -1 infection. Expand
The Probability of In Vivo Reactivation of Herpes Simplex Virus Type 1 Increases with the Number of Latently Infected Neurons in the Ganglia
  • N. Sawtell
  • Biology, Medicine
  • Journal of Virology
  • 1998
TLDR
The number of animals that exhibited virus reactivation was positively correlated with the number of latently infected neurons in the ganglia over the entire range examined and the relationship between herpes simplex virus latency and in vivo ganglionic reactivating was defined. Expand
Latent herpesvirus infection in human trigeminal ganglia causes chronic immune response.
TLDR
The persisting lymphocytic cell infiltration and the elevated CD8 and cytokine/chemokine expression in the TGs demonstrate for the first time that latent herpesviral infection in humans is accompanied by a chronic inflammatory process at an immunoprivileged site but without any neuronal destruction. Expand
...
1
2
3
4
5
...