PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 9608658

Does the latency associated transcript (LAT) of herpes simplex virus (HSV) function as a ribozyme during viral reactivation?

E K Hui·S J Lo
View original source ↗Export metadata ↓

Abstract

The latency associated transcript (LAT) of herpes simplex virus (HSV) appears to exist as an RNA molecule only. This phenomenon is consistent with the concept of functioning at an RNA level, and several lines of evidence suggest that the LAT may be a ribozyme. This provides an insight into understanding the role of LAT during HSV reactivation.

Explore related subjects

Herpesvirus 1, HumanHerpesvirus 2, HumanHumansRNA, CatalyticRNA, ViralVirus ActivationVirus LatencyJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

E K Hui, S J Lo. 1998. Does the latency associated transcript (LAT) of herpes simplex virus (HSV) function as a ribozyme during viral reactivation?. https://doi.org/10.1023/a%3A1007937521771

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2004

Human herpes simplex virus keratitis: the pathogenesis revisited.

Infections with several members of the human herpesviruses are the cause of significant ocular morbidity. Of the human herpesviruses, HSV-1 is the most frequent cause of primary and recurrent eye disease. Despite the availability of effective antiviral treatment, recurrent HSV-1 infection continues to be the leading cause of corneal blindness in industrialized nations. This review recapitulates the current insights in the role of the virus and the intra-corneal T cell response involved in the pathogenesis of human HSV-1-induced keratitis.

Herpesvirus 1, Human↗
PubMed2002

Transactivation of the human endogenous retrovirus K long terminal repeat by herpes simplex virus type 1 immediate early protein 0.

We found that LTR-directed transcription of the human endogenous retrovirus K can be induced by HSV-1 infection. The effect was mediated by the action of a HSV-1 immediate early protein, ICP0 and required the AP-1 binding site present on the HERV-K LTR. In addition, ICP0 could up-regulate AP-1 activity, suggesting that ICP0 increases transcription of HERV-K through AP-1 site. This effect might be important to understand both HERV-K- and HSV-1-mediated pathogenesis because HERV-K LTR represents an important class of retrotranspositional mutagens and also could provide a new regulatory element for the linked DNA sequences.

Herpesvirus 1, Human↗