Nectin-1-specific entry of herpes simplex virus 1 is sufficient for infection of the cornea and viral spread to the trigeminal ganglia.

Abstract

PURPOSE:

Primary and recurrent infections of the cornea by herpes simplex virus 1 (HSV-1) are important causes of eye disease. Three unrelated classes of glycoprotein D receptors for HSV-1 entry into cells have been identified. This study was undertaken to uncover the relative significance of nectin-1 as an entry receptor in corneal infection and HSV-1 spread to the trigeminal ganglia (TG), a site important for HSV-1 latency and recurrent corneal infection.

METHODS:

To assess the significance of nectin-1, a member of the immunoglobulin superfamily, in primary HSV-1 infection and spread to the TG, we used a murine model of corneal infection and a HSV-1 mutant, KOS(Rid1), which can only use nectin-1 for entry. Immunohistochemistry, real-time PCR, and plaque assays using HSV-1 infected tissues were performed.

RESULTS:

We demonstrated that receptor usage by HSV-1 limited to nectin-1 does not significantly change the spread of HSV-1 in the corneal epithelium during primary infection. We also found that nectin-1-specific entry does not affect the capacity of the virus to spread to the TG from the cornea.

CONCLUSIONS:

Our findings suggest that nectin-1 alone is sufficient for HSV-1 entry into the cornea and spread to the TG.

• Authors: Navika D Shukla, Vaibhav Tiwari, Tibor Valyi-Nagy
• Journal: Molecular vision (Mol Vis) Vol. 18 Pg. 2711-6 ( 2012) ISSN: 1090-0535 [Electronic] United States
• PMID: 23213272 (Publication Type: Journal Article)

Chemical References

• Cell Adhesion Molecules
• NECTIN1 protein, human
• Nectin1 protein, mouse
• Nectins
• Receptors, Virus

Topics

• Animals
• Cell Adhesion Molecules (genetics, metabolism)
• Disease Models, Animal
• Epithelium, Corneal (metabolism, pathology, virology)
• Gene Expression
• Herpes Simplex (metabolism, pathology, virology)
• Herpesvirus 1, Human (genetics, metabolism)
• Humans
• Immunohistochemistry
• Keratitis, Herpetic
• Mice
• Mice, Inbred BALB C
• Mutation
• Nectins
• Real-Time Polymerase Chain Reaction
• Receptors, Virus (genetics, metabolism)
• Trigeminal Ganglion (metabolism, pathology, virology)
• Viral Plaque Assay
• Virus Internalization
• Virus Latency
• Virus Replication