ArticleNucleic acids research1994
Inhibition of herpes simplex virus infection by ectopic expression of neuronal splice variants of the Oct-2 transcription factor.
Article in Nucleic acids research, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 23 citations in OpenAlex.
- The B-cell specific transcription factor, Oct-2, promotes Epstein-Barr virus latency by inhibiting the viral immediate-early protein, BZLF1.PLoS pathogens · 2012Article
- Herpes simplex virus type 1 and bovine herpesvirus 1 latency.Clinical microbiology reviews · 2003Review
- Herpes simplex virus type 1 latency-associated transcripts suppress viral replication and reduce immediate-early gene mRNA levels in a neuronal cell line.Journal of virology · 1998Article
- The TAATGARAT motif in the herpes simplex virus immediate-early gene promoters can confer both positive and negative responses to cellular octamer-binding proteins when it is located within the viral genome.Journal of virology · 1998Article
- Analysis of bovine herpesvirus 1 transcripts during a primary infection of trigeminal ganglia of cattle.Journal of virology · 1997Article
- Experimental investigation of herpes simplex virus latency.Clinical microbiology reviews · 1997Review
- The POU-domain factor Brn-3.0 recognizes characteristic sites in the herpes simplex virus genome.Nucleic acids research · 1997Article
- Transcription factors interacting with herpes simplex virus alpha gene promoters in sensory neurons.Nucleic acids research · 1995Article
- Neurons differentially control expression of a herpes simplex virus type 1 immediate-early promoter in transgenic mice.Journal of virology · 1995Article
- Quantification of transcripts from the ICP4 and thymidine kinase genes in mouse ganglia latently infected with herpes simplex virus.Journal of virology · 1995Article
- Functional differences between the Oct2 transactivation domains determine the transactivation potential of individual Oct2 isoforms.Nucleic acids research · 1994Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Herpes simplex virus (HSV) is capable of lytic replication in most cells, such replication in epithelial cells resulting in the mucocutaneous lesions observed following in vivo infection. In addition however, the virus also establishes asymptomatic latent infections in sensory neurons which serve as a reservoir for further cycles of peripheral lytic infections. These latent infections are dependent upon the inhibition of viral immediate-early (IE) gene expression via the octamer-related TAATGARAT motif in the IE promoters resulting in the failure of the viral lytic cycle. Here we show that the ectopic expression of neuronal isoforms of the octamer/TAATGARAT-binding transcription factor Oct-2 in permissive BHK cells represses IE gene expression following HSV infection and inhibits the viral lytic cycle whereas the B lymphocyte isoform of Oct-2 does not have this effect. These results suggest that the neuronal isoforms of Oct-2 play a critical role in rendering neuronal cells non-permissive for the viral lytic cycle thereby allowing the establishment of latent infection. Moreover, this is the first time that the ectopic expression of a cellular transcription factor has been shown to inhibit infection with any virus, raising the possibility of therapeutically inhibiting lytic viral infections by inducing such ectopic expression.
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