Herpes simplex virus (HSV), like all herpesviruses, is a formidable adversary with numerous strategies to evade the immune system. The fact that the virus is able to persist indefinitely in the host suggests that for most of the time the immune system is powerless to act. The anatomy of infection is a relatively simple process. HSV infects epithelial cells in the mucosa or skin, then enters peripheral nerve endings and travels intraaxonally to the sensory ganglia. It is in neurons that the virus establishes a latent infection, from which there may be a periodic reactivation. Here infectious virus reappears and travels back along nerve fibers to epidermal sites in skin where a new round of replication is initiated, referred to as a recurrent infection. During the primary infection, a strong immune response evolves composed of virus neutralizing antibodies and...
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1 May 2000
Commentary|
April 24 2000
T Cells and the Regulation of Herpes Simplex Virus Latency and Reactivation
Anthony A. Nash
Anthony A. Nash
aDepartment of Veterinary Pathology, University of Edinburgh, Edinburgh EH9 1QH, United Kingdom
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Anthony A. Nash
aDepartment of Veterinary Pathology, University of Edinburgh, Edinburgh EH9 1QH, United Kingdom
Received:
March 07 2000
Accepted:
March 20 2000
Online ISSN: 1540-9538
Print ISSN: 0022-1007
© 2000 The Rockefeller University Press
2000
The Rockefeller University Press
J Exp Med (2000) 191 (9): 1455–1458.
Article history
Received:
March 07 2000
Accepted:
March 20 2000
Citation
Anthony A. Nash; T Cells and the Regulation of Herpes Simplex Virus Latency and Reactivation. J Exp Med 1 May 2000; 191 (9): 1455–1458. doi: https://doi.org/10.1084/jem.191.9.1455
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