Related Experiment Video
Updated: May 1, 2026

A Primary Neuron Culture System for the Study of Herpes Simplex Virus Latency and Reactivation
Published on: April 2, 2012
Transactivation of a late herpes simplex virus promoter
Abstract:
We have asked whether the promoter for the gene encoding the major capsid protein (VP5) of herpes simplex virus functions in uninfected mouse cells. Our experimental strategy was to first fuse the VP5 promoter to the herpes simplex virus thymidine kinase (TK) structural sequence and then to use the resulting hybrid gene to transform TK- cells to TK+. The recombinant gene transferred TK at an extremely low frequency by comparison with the wild-type TK gene, and the TK transcripts present within the resulting rare transformants initiated within the TK structural gene, rather than in the vicinity of the VP5 promoter. However, after infection with herpes simplex virus, large amounts of RNA driven from the VP5 promoter accumulated. We conclude that the VP5 promoter does not function in uninfected cells but is efficiently activated by virally coded factors, most likely one or more immediate-early proteins.
More Related Videos
13:22Detection of the Genome and Transcripts of a Persistent DNA Virus in Neuronal Tissues by Fluorescent In situ Hybridization Combined with Immunostaining
Published on: January 23, 2014
08:26Purification of Viral DNA for the Identification of Associated Viral and Cellular Proteins
Published on: August 31, 2017
Related Concept Videos
Retrovirus Life Cycles
Retroviruses
LTR Retrotransposons
The internal coding region of LTR retrotransposons and their mechanism of transposition closely resembles a...
Mechanisms of Retrovirus-induced Cancers
Size and Structure of Viral Genomes