The herpes simplex virus type 1 (HSV-1) glycoprotein K(gK) is essential for viral corneal spread and

Andrew T David1, A Baghian, T P Foster

  • 1Division of Biotechnology and Molecular Medicine, School of Veterinary Medicine, Louisiana State University, Baton Rouge, Louisiana 70803, USA.

Current Eye Research
|June 24, 2008
PubMed
Abstract

Insights

Herpes simplex virus-1 glycoprotein K (gK) is crucial for viral spread in the cornea and invasion of the trigeminal ganglia. Deleting gK in HSV-1 prevents corneal infection and neuroinvasion in mice.

Area of Science:

  • Virology
  • Ophthalmology
  • Neuroscience

Background:

  • Herpes simplex virus-1 (HSV-1) establishes lifelong latency, often in the trigeminal ganglia.
  • Reactivation of HSV-1 can lead to ocular disease, such as keratitis.
  • The role of specific viral proteins in HSV-1 pathogenesis is critical for understanding infection dynamics.

Purpose of the Study:

  • To investigate the function of HSV-1 glycoprotein K (gK) in ocular infection.
  • To determine the role of gK in viral neuroinvasion to the trigeminal ganglia.
  • To assess the impact of gK on HSV-1 latency establishment.

Main Methods:

  • Construction of a recombinant HSV-1 (McKrae) Delta gK (MKDelta gK) virus with a deleted gK gene.
  • Ocular infection of Balb/c mice with MKDelta gK and a rescued wild-type-like virus (MKgK).
  • Monitoring of corneal infection spread, clinical disease, and viral DNA detection in trigeminal ganglia via PCR.

Main Results:

  • Mice infected with MKDelta gK showed no clinical signs, unlike those infected with MKgK.
  • MKDelta gK failed to spread in mouse corneas, whereas MKgK spread efficiently.
  • HSV DNA was detected in trigeminal ganglia of MKgK-infected mice but rarely in MKDelta gK-infected mice.

Conclusions:

  • HSV-1 gK is essential for efficient viral replication and spread within the corneal epithelium.
  • gK plays a critical role in HSV-1 neuroinvasion into the trigeminal ganglia.
  • The absence of gK significantly impairs the establishment of HSV-1 infection and latency.

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