Corneal replication is an interferon response-independent bottleneck for virulence of herpes simplex virus 1 in the absence of virion host shutoff

Tracy Jo Pasieka, Vineet Menachery, Pamela C. Rosato, David A. Leib

Research output: Contribution to journalArticle

8 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)7692-7695
Number of pages4
JournalJournal of Virology
Volume86
Issue number14
DOIs
StatePublished - Jul 1 2012
Externally publishedYes

Fingerprint

Human herpesvirus 1
Human Herpesvirus 1
interferons
virion
Virion
Interferons
Virulence
virulence
herpes simplex
Interferon Type I
Simplexvirus
Infection
interferon-gamma
infection
Interferon-gamma
viruses
mice

ASJC Scopus subject areas

  • Immunology
  • Virology

Cite this

Corneal replication is an interferon response-independent bottleneck for virulence of herpes simplex virus 1 in the absence of virion host shutoff. / Pasieka, Tracy Jo; Menachery, Vineet; Rosato, Pamela C.; Leib, David A.

In: Journal of Virology, Vol. 86, No. 14, 01.07.2012, p. 7692-7695.

Research output: Contribution to journalArticle

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