Corneal Replication Is an Interferon Response-Independent Bottleneck for Virulence of Herpes Simplex Virus 1 in the Absence of Virion Host Shutoff

Authors

Tracy J. Pasieka, Washington University School of Medicine
Vineet D. Menachery, Washington University School of Medicine
Pamela C. Rosato, Dartmouth College
David A. Leib, Dartmouth College

Document Type

Article

Publication Date

5-2-2012

Publication Title

Journal of Virology

Department

Geisel School of Medicine

Abstract

Herpes simplex viruses lacking the virion host shutoff function (Δvhs) are avirulent and hypersensitive to type I and type II interferon (IFN). In this study, we demonstrate that even in the absence of IFN responses in AG129 (IFN-αβγR^−/−) mice, Δvhs remains highly attenuated via corneal infection but is fully virulent via intracranial infection. The data demonstrate that the interferon-independent inherent replication defect of Δvhs has a significant impact upon peripheral replication and neuroinvasion.

DOI

10.1128/JVI.00761-12

Original Citation

Pasieka TJ, Menachery VD, Rosato PC, Leib DA. Corneal replication is an interferon response-independent bottleneck for virulence of herpes simplex virus 1 in the absence of virion host shutoff. J Virol. 2012 Jul;86(14):7692-5. doi: 10.1128/JVI.00761-12. Epub 2012 May 2. PMID: 22553331; PMCID: PMC3416281.

Dartmouth Digital Commons Citation

Pasieka, Tracy J.; Menachery, Vineet D.; Rosato, Pamela C.; and Leib, David A., "Corneal Replication Is an Interferon Response-Independent Bottleneck for Virulence of Herpes Simplex Virus 1 in the Absence of Virion Host Shutoff" (2012). Dartmouth Scholarship. 1231.
https://digitalcommons.dartmouth.edu/facoa/1231