Corneal replication is an interferon response-independent bottleneck for virulence of herpes simplex virus 1 in the absence of virion host shutoff.
J Virol
; 86(14): 7692-5, 2012 Jul.
Article
in En
| MEDLINE
| ID: mdl-22553331
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-αßγR(-/-)) 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.
Full text:
1
Database:
MEDLINE
Main subject:
Ribonucleases
/
Viral Proteins
/
Interferon Type I
/
Interferon-gamma
/
Keratitis, Herpetic
/
Herpesvirus 1, Human
/
Cornea
Limits:
Animals
Language:
En
Journal:
J Virol
Year:
2012
Type:
Article
Affiliation country:
United States