Herpes virus latency in sensory ganglia--a comparison with endogenous neuronal gene expression.
Prog Neurobiol
; 60(2): 167-79, 2000 Feb.
Article
em En
| MEDLINE
| ID: mdl-10639053
Central to infection by a majority of DNA viruses is the expression of encoded proteins that modify cell cycle. Viruses such as SV40 and Adenovirus viruses encode proteins that interact directly, or indirectly, with key cell cycle proteins such as CBP300 and the retinoblastoma gene product. However, neurons do not have a cell cycle as we generally describe it and this is also reflected in the difficulty in obtaining immortalised neuronal cultures. The replication strategies of viruses that infect post-mitotic cells such as neurons may be different from infection of other somatic cells. The life cycle for viral latency or slow infection of neurons appears to involve silencing or restricting expression of the viral genome until such times as dictated by the environment. These signals from the environment usually reflect cell stress, otherwise the cell appears to tolerate the existence of the virus genome. We will review the genomic structure of alphaherpesviruses in neurons and transcriptional control mechanisms that may regulate expression. Where appropriate we will contrast and compare virus and endogenous neuronal gene expression.
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Coleções:
01-internacional
Temas:
Geral
Base de dados:
MEDLINE
Assunto principal:
Regulação Viral da Expressão Gênica
/
Latência Viral
/
Herpesvirus Humano 1
/
Gânglios Sensitivos
/
Herpes Simples
/
Neurônios
Limite:
Animals
/
Humans
Idioma:
En
Revista:
Prog Neurobiol
Ano de publicação:
2000
Tipo de documento:
Article