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

doi:10.1128/JVI.00761-12

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 journal › Article › peer-review

9 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 language	English (US)
Pages (from-to)	7692-7695
Number of pages	4
Journal	Journal of virology
Volume	86
Issue number	14
DOIs	https://doi.org/10.1128/JVI.00761-12
State	Published - Jul 2012
Externally published	Yes

ASJC Scopus subject areas

Microbiology
Immunology
Insect Science
Virology

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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.",

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AU - Rosato, Pamela C.

AU - Leib, David A.

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AB - 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.

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

Abstract

ASJC Scopus subject areas

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