Cd8+ T Cells Can Block Herpes Simplex Virus Type 1 (HSV-1) Reactivation from Latency in Sensory Neurons

DOI PDF 被引用文献2件
  • Ting Liu
    aDepartment of Ophthalmology, University of Pittsburgh, School of Medicine, Pittsburgh, Pennsylvania 15213
  • Kamal M. Khanna
    aDepartment of Ophthalmology, University of Pittsburgh, School of Medicine, Pittsburgh, Pennsylvania 15213
  • XiaoPing Chen
    bDepartment of Neurology, University of Pittsburgh, School of Medicine, Pittsburgh, Pennsylvania 15213
  • David J. Fink
    bDepartment of Neurology, University of Pittsburgh, School of Medicine, Pittsburgh, Pennsylvania 15213
  • Robert L. Hendricks
    aDepartment of Ophthalmology, University of Pittsburgh, School of Medicine, Pittsburgh, Pennsylvania 15213

書誌事項

公開日
2000-04-24
DOI
  • 10.1084/jem.191.9.1459
公開者
Rockefeller University Press

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<jats:p>Recurrent herpes simplex virus type 1 (HSV-1) disease usually results from reactivation of latent virus in sensory neurons and transmission to peripheral sites. Therefore, defining the mechanisms that maintain HSV-1 in a latent state in sensory neurons may provide new approaches to reducing susceptibility to recurrent herpetic disease. After primary HSV-1 corneal infection, CD8+ T cells infiltrate the trigeminal ganglia (TGs) of mice, and are retained in latently infected ganglia. Here we demonstrate 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. Latently infected neurons expressed viral genome and some expressed HSV-1 immediate early and early proteins, but did not produce HSV-1 late proteins or infectious virions. Addition of anti-CD8α monoclonal antibody 5 d after culture initiation induced HSV-1 reactivation, as demonstrated by production of viral late proteins and infectious virions. Thus, CD8+ T cells can prevent HSV-1 reactivation without destroying the infected neurons. We propose 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.</jats:p>

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