Influence of Herpes Simplex Virus 1 Latency-Associated Transcripts on the Establishment and Maintenance of Latency in the ROSA26R Reporter Mouse Model
| Autor: | Michael P. Nicoll, Viv Connor, Stacey Efstathiou, João T. Proença |
|---|---|
| Rok vydání: | 2012 |
| Předmět: |
Gene Expression Regulation
Viral Transcription Genetic viruses Immunology Cell Population Herpesvirus 1 Human Biology medicine.disease_cause Microbiology Cell Line law.invention Mice law Cricetinae Virology Virus latency medicine Animals Latency (engineering) skin and connective tissue diseases education education.field_of_study biochemical phenomena metabolism and nutrition medicine.disease Phenotype Virus Latency medicine.anatomical_structure Herpes simplex virus nervous system Cell culture Insect Science Recombinant DNA Pathogenesis and Immunity Female Ganglia |
| Zdroj: | Journal of Virology. 86:8848-8858 |
| ISSN: | 1098-5514 0022-538X |
| DOI: | 10.1128/jvi.00652-12 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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