|
|
|
|
|
|
|
||
J. Exp. Med.,
Volume 187, Number 3, February 2, 1998 341-348
By
From the * Department of Molecular Microbiology and Immunology, Oregon Health Sciences
University, Portland, Oregon 97201, and the The herpes simplex virus (HSV) infected cell protein (ICP)47 blocks CD8+ T cell recognition
of infected cells by inhibiting the transporter associated with antigen presentation (TAP). In
vivo, HSV-1 replicates in two distinct tissues: in epithelial mucosa or epidermis, where the virus enters sensory neurons; and in the peripheral and central nervous system, where acute and
subsequently latent infections occur. Here, we show that an HSV-1 ICP47 Department of Ophthalmology and Visual Sciences,
and the Department of Pathology, University of Illinois at Chicago, Chicago, Illinois 60612
mutant is less neurovirulent than wild-type HSV-1 in mice, but replicates normally in epithelial tissues. The reduced neurovirulence of the ICP47 mutant was due to a protective CD8+ T cell response.
When compared with wild-type virus, the ICP47 mutant expressed reduced neurovirulence
in immunologically normal mice, and T cell-deficient nude mice after reconstitution with CD8+ T cells. However, the ICP47 mutant exhibited normal neurovirulence in mice that
were acutely depleted of CD8+ T cells, and in nude mice that were not reconstituted, or were reconstituted with CD4+ T cells. In contrast, CD8+ T cell depletion did not increase the neurovirulence of an unrelated, attenuated HSV-1 glycoprotein (g)E mutant. ICP47 is the first
viral protein shown to influence neurovirulence by inhibiting CD8+ T cell protection.
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
This article has been cited by other articles:
| TABLE OF CONTENTS |
|
