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Updated: Jul 4, 2026

Ex Vivo Infection of Murine Epidermis with Herpes Simplex Virus Type 1
Published on: August 24, 2015
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.
Purpose:
To determine the role of herpes simplex virus-1 (HSV-1) glycoprotein K(gK) in corneal infection, neuroinvasion, and virus latency in trigeminal ganglia of mice.
Methods:
The recombinant virus HSV-1 (McKrae) Delta gK (MKDelta gK) carrying a deletion of the gK gene was constructed by insertional/deletion mutagenesis and replaced by a gene cassette constitutively expressing the enhanced green fluorescence protein. The gK deletion of the MKDelta gK virus was rescued to produce the wild-type-like virus MKgK. Balb/c mice were infected ocularly with either virus, and the infection pattern in the eye, clinical disease progression, and establishment of viral latency was monitored.
Results:
Mice infected with the MKDelta gK strain produced in a gK complementing cell line did not exhibit clinical signs when compared with mice infected with the MKgK virus. Direct visualization of infected eyes revealed that the MKDelta gK virus was unable to spread in mouse corneas, while the MKgK rescued virus spread efficiently. Nineteen of 20 scarified and 5/12 unscarified mice infected with the MKgK virus produced infectious virus after coculture with permissive cells, while 0/20 scarified and 0/12 unscarified mice infected with the MKDelta gK virus produced infectious virus. HSV DNA was detected in trigeminal ganglia by PCR in 19/20 scarified and 9/12 unscarified mice inoculated with MKgK, while HSV DNA was detected in the trigeminal ganglia of 3/20 scarified and 0/12 unscarified mice inoculated with MKDelta gK.
Conclusions:
The results show that HSV-1 gK is essential for efficient replication and spread in the corneal epithelium and trigeminal ganglia neuroinvasion in MKDelta gK inoculated mice.
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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