Recurrent HSV-I, due to reactivation of latent virus from sensory neurons, is a major cause of corneal blindness. LAT, the only viral transcript thought to be made during latency, is essential for efficient reactivation. Recently, a new viral transcript, AL, was found during latency. AL is anti-sense to LAT and produces a protein in infected rabbits. Since AL and LAT overlap, phenotypes previously attributed to LAT may be due to AL. Two hypotheses will be tested: AL plays a role in (1) spontaneous reactivation; and (2) virulence.
My specific aim i s to determine the function of AL. AL-/LAT + and AL+/LAT - mutants will be constructed and their reactivation and virulence phenotypes analyzed in the rabbit ocular model. These complementary mutants should allow us to determine if AL is involved in spontaneous reactivation and/or virulence, or if both phenotypes are due solely to LAT. This information will be critical to the development of novel strategies to reduce recurrent viral reactivation and conseequently reduce HSV-1 induced eye disease.

Agency
National Institute of Health (NIH)
Institute
National Eye Institute (NEI)
Type
Postdoctoral Individual National Research Service Award (F32)
Project #
1F32EY014512-01A1
Application #
6694910
Study Section
Special Emphasis Panel (ZRG1-F08 (20))
Program Officer
Shen, Grace L
Project Start
2003-08-01
Project End
2006-07-31
Budget Start
2003-08-01
Budget End
2004-07-31
Support Year
1
Fiscal Year
2003
Total Cost
$46,420
Indirect Cost
Name
University of California Irvine
Department
Ophthalmology
Type
Schools of Medicine
DUNS #
046705849
City
Irvine
State
CA
Country
United States
Zip Code
92697
Jin, Ling; Perng, Guey-Chuen; Brick, David J et al. (2004) Methods for detecting the HSV-1 LAT anti-apoptosis activity in virus infected tissue culture cells. J Virol Methods 118:9-13