Immune control of herpes simplex virus during latency.
Herpes simplex virus type 1 (HSV-1) persists within the host in the presence of concomitant immunity by establishing a latent infection within sensory neurons. HSV-1 latency is widely viewed as a neuron-enforced quiescent state of the virus, in which a lack of viral protein synthesis prevents recognition of the infected neuron by the host immune system. On the basis of recent findings, however, we propose a more dynamic view of HSV-1 latency characterized by persistent or intermittent low-level viral gene expression in some latently infected neurons. We further propose that HSV-1-specific memory/effector CD8(+) T lymphocytes that are retained in the ganglion in close apposition to the neurons prevent full reactivation and virion formation through IFN-gamma production and an additional undefined mechanism(s).
Khanna
Kamal M
KM
Graduate Program in Immunology, Department of Ophthalmology, University of Pittsburgh, 203 Lothrop Street, Pittsburgh, PA 15213-2588, USA.
Lepisto
Andrew J
AJ
Decman
Vilma
V
Hendricks
Robert L
RL
D018414:CD8-Positive T-Lymphocytes / Q000276:immunology*; D017950:Ganglia, Sensory / Q000276:immunology / Q000821:virology; D015967:Gene Expression Regulation, Viral / Q000276:immunology; D006566:Herpesviridae Infections / Q000276:immunology* / Q000821:virology; D018259:Herpesvirus 1, Human / Q000276:immunology*; D006801:Humans; D007156:Immunologic Memory; D009475:Neurons, Afferent / Q000276:immunology* / Q000821:virology; D014764:Viral Proteins / Q000276:immunology; D017735:Virus Latency / Q000276:immunology*; D014779:Virus Replication / Q000276:immunology
D014764:Viral Proteins