Innate and acquired immunity to herpes simplex virus type 1.

Abstract:

:Immunization with heat-inactivated herpes simplex virus type 1 (HSV-1) 2-5 days before ocular infection reduced the frequency of establishment of latent HSV-1 infection in the trigeminal ganglion (TG); this induction of resistance coincided with reduced expression of IFN-gamma mRNA in the TG. Immunization with unrelated antigens was not protective. In part, this resistance to nervous system invasion correlated with the appearance of serum antibody to HSV-1. Immunization reduced viral replication in the eye and trigeminal ganglion, and prevented HSV-1 spread to the cerebellum. IFN-gamma was detected in immunized mice 4 days postocular infection as determined by plaque reduction using neutralizing Ab to IFN-alpha/beta and IFN-gamma. Injection of antibody (Ab) to IFN-alpha/beta and IFN-gamma administered at the time of immunization did not affect survival. Anti-IFN-gamma-treated mice had significantly reduced levels of IFN in their serum. Treatment with anti-IFN-alpha/beta Ab resulted in an elevation in viral replication as determined by the expression of latency associated transcripts in the TG of mice. Likewise, there was a significant increase in the CD8, IL-12 (p40), and TNF-alpha mRNA levels in the TG of the anti-IFN-alpha/beta-treated mice TG explant cultures demonstrated that viral load was significantly increased in the TG of anti-IFN-alpha/beta-treated mice relative to TG of control mice 7 days after infection. The results suggest that exposure to viral antigens 2-5 days before infection is an important determinant of the extent of HSV-1 spread to the nervous system. Moreover, the data suggest that both an antibody response and IFN-alpha/beta play a role in limiting the progress of infection from the peripheral tissues to the central nervous system.

journal_name

Virology

journal_title

Virology

authors

Halford WP,Veress LA,Gebhardt BM,Carr DJ

doi

10.1006/viro.1997.8738

subject

Has Abstract

pub_date

1997-09-29 00:00:00

pages

328-37

issue

2

eissn

0042-6822

issn

1096-0341

pii

S0042-6822(97)98738-9

journal_volume

236

pub_type

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