Deletion of the S component inverted repeat sequencec′ and the nonessential genes Us1 through Us5 from the herpes simplex virus type 1 genome substantially impairs productive viral infection in cell culture and pathogenesis in the rat central nervous system

1997 ◽  
Vol 3 (4) ◽  
pp. 247-264 ◽  
Author(s):  
Siyamak Rasty ◽  
P Luigi Poliani ◽  
David J Fink ◽  
Joseph C Glorioso
Keyword(s):  
Central Nervous System ◽  
Cell Culture ◽  
Nervous System ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Viral Infection ◽  
Herpes Simplex Virus Type ◽  
Inverted Repeat ◽  
Simplex Virus

scholarly journals Interferon Regulatory Factor 3-Dependent Pathways Are Critical for Control of Herpes Simplex Virus Type 1 Central Nervous System Infection

2010 ◽  
Vol 84 (19) ◽  
pp. 9685-9694 ◽  
Author(s):  
Vineet D. Menachery ◽  
Tracy Jo Pasieka ◽  
David A. Leib
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Viral Infection ◽  
Central Nervous System Infection ◽  
Regulatory Factor ◽  
Simplex Virus ◽  
Hsv 1

ABSTRACT The initiation of the immune response at the cellular level relies on specific recognition molecules to rapidly signal viral infection via interferon (IFN) regulatory factor 3 (IRF-3)-dependent pathways. The absence of IRF-3 would be expected to render such pathways inoperative and thereby significantly affect viral infection. Unexpectedly, a previous study found no significant change in herpes simplex virus (HSV) pathogenesis in IRF-3−/− mice following intravenous HSV type 1 (HSV-1) challenge (K. Honda, H. Yanai, H. Negishi, M. Asagiri, M. Sato, T. Mizutani, N. Shimada, Y. Ohba, A. Takaoka, N. Yoshida, and T. Taniguchi, Nature 434:772-777, 2005). In contrast, the present study demonstrated that IRF-3−/− mice are significantly more susceptible to HSV infection via the corneal and intracranial routes. Following corneal infection with 2 × 106 PFU of HSV-1 strain McKrae, 50% of wild-type mice survived, compared to 10% of IRF-3-deficient mice. Significantly increased viral replication and inflammatory cytokine production were observed in brain tissues of IRF-3−/− mice compared to control mice, with a concomitant deficit in production of both IFN-β and IFN-α. These data demonstrate a critical role for IRF-3 in control of central nervous system infection following HSV-1 challenge. Furthermore, this work underscores the necessity to evaluate multiple routes of infection and animal models in order to fully determine the role of host resistance factors in pathogenesis.

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