CD8+ T cells patrol HSV-1-infected trigeminal ganglia and prevent viral reactivation
AJ St. Leger, RL Hendricks - Journal of neurovirology, 2011 - Springer
Journal of neurovirology, 2011•Springer
A hallmark of herpes viruses is their capacity to cause recurrent disease. Recurrences of
herpes simplex virus (HSV)-1 disease do not result from reinfection from external sources,
but rather from reactivation of virus that is maintained in a latent state in sensory neurons
and periodically reactivates from latency to cause recurrent disease. Recent findings
implicate HSV-specific CD8+ T cells in immune surveillance of HSV-1 latently infected
sensory neurons in trigeminal ganglia (TG) and inhibition of HSV-1 reactivation from latency …
herpes simplex virus (HSV)-1 disease do not result from reinfection from external sources,
but rather from reactivation of virus that is maintained in a latent state in sensory neurons
and periodically reactivates from latency to cause recurrent disease. Recent findings
implicate HSV-specific CD8+ T cells in immune surveillance of HSV-1 latently infected
sensory neurons in trigeminal ganglia (TG) and inhibition of HSV-1 reactivation from latency …
Abstract
A hallmark of herpes viruses is their capacity to cause recurrent disease. Recurrences of herpes simplex virus (HSV)-1 disease do not result from reinfection from external sources, but rather from reactivation of virus that is maintained in a latent state in sensory neurons and periodically reactivates from latency to cause recurrent disease. Recent findings implicate HSV-specific CD8+ T cells in immune surveillance of HSV-1 latently infected sensory neurons in trigeminal ganglia (TG) and inhibition of HSV-1 reactivation from latency. This review summarizes recent findings regarding the characteristics of the TG-resident CD8+ T cell population and certain unique obstacles that might complicate the development of therapeutic vaccines.
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