Histone deacetylase inhibitors suppress coxsackievirus B3 growth in vitro and myocarditis induced in mice
| Autor: | Jae-Hwan Nam, Ye Mb, Park Jh, Shim Sh |
|---|---|
| Rok vydání: | 2013 |
| Předmět: |
Male
Viral Myocarditis viruses Coxsackievirus Infections Histone Deacetylase 2 Coxsackievirus Hydroxamic Acids Virus Replication chemistry.chemical_compound Mice Virology medicine Enterovirus Infections Animals Humans Mice Inbred BALB C biology Histone deacetylase 2 virus diseases General Medicine Histone acetyltransferase biology.organism_classification Enterovirus B Human Histone Deacetylase Inhibitors Myocarditis Infectious Diseases Histone Trichostatin A chemistry biology.protein Cancer research Histone deacetylase Apicidin medicine.drug HeLa Cells |
| Zdroj: | Acta virologica. 57(4) |
| ISSN: | 0001-723X |
| Popis: | UNLABELLED Clinical importance of myocarditis, predominantly caused by coxsackievirus B3 (CVB3), is recently rising. However, a detailed mechanism of pathogenesis of CVB3 myocarditis still needs to be clarified. Recently, it has been reported that histone modifications including acetylation are involved in coxsackievirus replication. To examine whether the CVB3 replication requires histone acetylation, histone deacetylase (HDAC) inhibitors were employed. We found that the HDAC2 activity increased in virus-infected cells at 12 hrs p.i. and that HDAC inhibitors suppressed the virus replication in vitro. This suggests that the HDAC2 activity may be required for the virus replication. Eventually, a HDAC inhibitor trichostatin A protected against CVB3-induced myocardial injury in vivo. Our results suggest that HDAC may be a novel therapeutic target for treating viral myocarditis. KEYWORDS coxsackievirus B3; histone acetyltransferase; histone deacetylase; HDAC inhibitors, trichostatin A; apicidin; valproic acid; shRNA; myocarditis; mouse. |
| Databáze: | OpenAIRE |
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