The Region of the HSV-1 Latency-Associated Transcript Required for Epinephrine-Induced Reactivation in the Rabbit Does Not Include the 2.0-kb Intron

• Published in: Virology (New York, N.Y.) Vol. 292; no. 1; pp. 59 - 69
• Main Authors: Jarman, Richard G., Loutsch, Jeannette M., Devi-Rao, Gayathri B., Marquart, Mary E., Banaszak, Matthew P., Zheng, Xiaodong, Hill, James M., Wagner, Edward K., Bloom, David C.
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 05.01.2002
• Subjects: Animals; Disease Models, Animal; Epinephrine - pharmacology; Gene Deletion; Herpes simplex virus 1; Herpesvirus 1, Human - genetics; Herpesvirus 1, Human - physiology; herpesvirus, latency, reactivation, latency-associated transcript; Humans; Introns; Keratitis, Herpetic - virology; LAT gene; Rabbits; Transcription, Genetic; Viral Proteins - genetics; Viral Proteins - metabolism; Virus Activation - drug effects; Virus Latency; herpesvirus, latency, reactivation, latency-associated transcript
• DOI: 10.1006/viro.2001.1265
• ISSN: 0042-6822

Previous studies have localized the region of the latency-associated transcript (LAT) of HSV-1 responsible for epinephrine-induced reactivation in the rabbit eye model to the first 1.5 kb of the primary transcript. This region extends from the 5′ exon of the primary LAT transcript through the 5′ half of the LAT 2.0-kb intron. To determine whether the 5′ end of the LAT intron contributes to the induced reactivation phenotype, three recombinant viruses containing deletions within this portion of the LAT intron were constructed. The three recombinants, containing deletions spanning a combined region of 969 bp at the 5′ end of the LAT intron, reactivated with the wild-type frequency of 17syn+. These results indicate that the elements governing induced reactivation reside within the first 699 bp of the primary LAT transcript encoding the 5′ LAT exon.