Abstract |
Herpes simplex virus 1 (HSV-1) can establish life-long latent infection in sensory neurons, from which periodic reactivation can occur. During latency, viral gene expression is largely restricted to the latency-associated transcripts ( LATs). While not essential for any phase of latency, to date the LATs have been shown to increase the efficiency of both establishment and reactivation of latency in small-animal models. We sought to investigate the role of LAT expression in the frequency of latency establishment within the ROSA26R reporter mouse model utilizing Cre recombinase-encoding recombinant viruses harboring deletions of the core LAT promoter (LAP) region. HSV-1 LAT expression was observed to influence the number of latently infected neurons in trigeminal but not dorsal root ganglia. Furthermore, the relative frequencies of latency establishment of LAT-positive and LAT-negative viruses are influenced by the inoculum dose following infection of the mouse whisker pads. Finally, analysis of the infected cell population at two latent time points revealed a relative loss of latently infected cells in the absence of LAT expression. We conclude that the HSV-1 LATs facilitate the long-term stability of the latent cell population within the infected host and that interpretation of LAT establishment phenotypes is influenced by infection methodology.
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Authors | M P Nicoll, J T Proença, V Connor, S Efstathiou |
Journal | Journal of virology
(J Virol)
Vol. 86
Issue 16
Pg. 8848-58
(Aug 2012)
ISSN: 1098-5514 [Electronic] United States |
PMID | 22696655
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Topics |
- Animals
- Cell Line
- Cricetinae
- Female
- Ganglia
(virology)
- Gene Expression Regulation, Viral
- Herpesvirus 1, Human
(pathogenicity, physiology)
- Mice
- Transcription, Genetic
- Virus Latency
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