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 D. Menachery, Pamela C. Rosato, David A. Leib

Research output: Contribution to journalArticlepeer-review

8 Scopus citations

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 2012
Externally publishedYes

ASJC Scopus subject areas

  • Microbiology
  • Immunology
  • Insect Science
  • Virology

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