Decreased reactivation of a herpes simplex virus type 1 (HSV-1) latency-associated transcript (LAT) mutant using the in vivo mouse UV-B model of induced reactivation
| Autor: | Nelson Osorio, Steven L. Wechsler, Arif A. Khan, Jennifer Simpson, Ruchi Srivastava, Lbachir BenMohamed |
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| Rok vydání: | 2015 |
| Předmět: |
Ultraviolet Rays
viruses Mutant Herpesvirus 1 Human Biology medicine.disease_cause Article Virus Mice Cellular and Molecular Neuroscience Immune system In vivo Virology Virus latency Medicine and Health Sciences medicine Animals Virus Activation medicine.disease Phenotype Virus Latency Mice Inbred C57BL Disease Models Animal MicroRNAs Herpes simplex virus Neurology Keratitis Herpetic Female Neurology (clinical) |
| Zdroj: | BenMohamed, Lbachir; Osorio, Nelson; Srivastava, Ruchi; Khan, Arif A; Simpson, Jennifer L; & Wechsler, Steven L. (2015). Decreased reactivation of a herpes simplex virus type 1 (HSV-1) latency-associated transcript (LAT) mutant using the in vivo mouse UV-B model of induced reactivation. Journal of NeuroVirology, 21(5), 508-517. doi: 10.1007/s13365-015-0348-9. UC Irvine: Institute for Clinical and Translational Science. Retrieved from: http://www.escholarship.org/uc/item/2sr083j6 |
| ISSN: | 1538-2443 1355-0284 |
| DOI: | 10.1007/s13365-015-0348-9 |
| Popis: | Blinding ocular herpetic disease in humans is due to herpes simplex virus type 1 (HSV-1) reactivations from latency, rather than to primary acute infection. The cellular and molecular immune mechanisms that control the HSV-1 latency-reactivation cycle remain to be fully elucidated. The aim of this study was to determine if reactivation of the HSV-1 latency-associated transcript (LAT) deletion mutant (dLAT2903) was impaired in this model, as it is in the rabbit model of induced and spontaneous reactivation and in the trigeminal ganglia (TG) explant-induced reactivation model in mice. The eyes of mice latently infected with wild-type HSV-1 strain McKrae (LAT((+)) virus) or dLAT2903 (LAT((-)) virus) were irradiated with UV-B, and reactivation was determined. We found that compared to LAT((-)) virus, LAT((+)) virus reactivated at a higher rate as determined by shedding of virus in tears on days 3 to 7 after UV-B treatment. Thus, the UV-B-induced reactivation mouse model of HSV-1 appears to be a useful small animal model for studying the mechanisms involved in how LAT enhances the HSV-1 reactivation phenotype. The utility of the model for investigating the immune evasion mechanisms regulating the HSV-1 latency/reactivation cycle and for testing the protective efficacy of candidate therapeutic vaccines and drugs is discussed. |
| Databáze: | OpenAIRE |
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