Abstract
During herpes simplex virus-1 (HSV-1) latency in sensory neurons, LAT (latency-associated transcript) is the only abundantly expressed viral gene. LAT plays an important role in the HSV-1 latency-reactivation cycle, because LAT deletion mutants have a significantly decreased reactivation phenotype. Based solely on sequence analysis, it was speculated that LAT encodes a ribozyme that plays an important role in how LAT enhances the virus’ reactivation phenotype. Because LAT ribozyme activity has never been reported, we decided to test the converse hypothesis, namely, that this region of LAT does not encode a ribozyme function important for LAT's ability to enhance the reactivation phenotype. We constructed a viral mutant (LAT-Rz) in which the speculated ribozyme consensus sequence was altered such that no ribozyme was encoded. We report here that LAT-Rz had a wild-type reactivation phenotype in mice, confirming the hypothesis that the speculated LAT ribozyme is not a dominant factor in stimulating the latency-reactivation cycle in mice.
Acknowledgements
This work was supported by Public Health Service grants EY013191, EY018171, EY016663, 1P20RR15635, and R21AI069176, USDA grants 2005-01554 and 2006-01627, the Discovery Eye Foundation, the Skirball Program in Molecular Ophthalmology, and Research to Prevent Blindness. S.L.W. is an RPB Senior Scientific Investigator.
Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.