May 2006
Volume 47, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2006
A Role for Autophagy in the Control of Growth of Herpes Simplex Virus Type 1
Author Affiliations & Notes
  • D.A. Leib
    Ophthalmology, Molecular Microbiology, Washington University, St. Louis, MO
  • S.L. Ward
    Ophthalmology, Molecular Microbiology, Washington University, St. Louis, MO
  • B. Levine
    Division of Infectious Diseases, University of Texas Souwestern Medical Center, Dallas, TX
  • Footnotes
    Commercial Relationships  D.A. Leib, None; S.L. Ward, None; B. Levine, None.
  • Footnotes
    Support  NIH EY09083, Research to Prevent Blindness.
Investigative Ophthalmology & Visual Science May 2006, Vol.47, 2655. doi:
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      D.A. Leib, S.L. Ward, B. Levine; A Role for Autophagy in the Control of Growth of Herpes Simplex Virus Type 1 . Invest. Ophthalmol. Vis. Sci. 2006;47(13):2655.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: : To assess the role of cellular autophagy in the regulation of replication of herpes simplex virus type 1 and to assess the abilty of the neurovirulence gene ICP34.5 to prevent autophagy.

Methods: : We used a small nucleotide analog, 3–methyladenine (3–MA), which inhibits autophagy at an early step in autophagosome formation. Additionally, we used cells with tightly regulated Atg5 expression to provide a genetic correlate to the drug–treatment experiments. We also analyzed the relationship between the ability of ICP34.5 to prevent translational arrest through its dephosphorylation of eIF2α and its prevention of autophagy.

Results: : We show that 3–MA rescues the ability of a virus lacking ICP34.5 to replicate in vitro. Cells lacking Atg5 activity were also much more permissive for replication of an ICP34.5–deficient virus than control cells. In addition, 3–MA treatment, while having no effect on the eIF2α phosphorylation, increased protein accumulation in cells infected with an ICP34.5–null mutant

Conclusions: : These data show that the growth of an ICP34.5 mutant is regulated by autophagy and that regulation of the autophagy pathway is a pivotal determinant of efficient viral replication.

Keywords: herpes simplex virus • immunomodulation/immunoregulation 
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