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Journal of Virology, October 2001, p. 9596-9600, Vol. 75, No. 20
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.20.9596-9600.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Interleukin-12- and Gamma Interferon-Dependent Innate Immunity Are Essential and Sufficient for Long-Term Survival of Passively Immunized Mice Infected with Herpes Simplex Virus Type 1

Sabine Vollstedt,1 Marco Franchini,1 Gottfried Alber,2 Mathias Ackermann,1 and Mark Suter1,*

Institute of Virology, University of Zurich, Zurich, Switzerland,1 and Institute of Immunology, Faculty of Veterinary Medicine, University of Leipzig, Leipzig, Germany2

Received 16 April 2001/Accepted 12 July 2001

Interferon (IFN) type I (alpha/beta IFN [IFN-alpha /beta ]) is very important in directly controlling herpes simplex virus type I (HSV-1) replication as well as in guiding and upregulating specific immunity against this virus. By contrast, the roles of IFN type II (IFN-gamma ) and antibodies in the defense against HSV-1 are not clear. Mice without a functional IFN system and no mature B and T cells (AGR mice) did not survive HSV-1 infection in the presence or absence of neutralizing antibodies to the virus. Mice without a functional IFN type I system and with no mature B and T cells (AR129 mice) were unable to control infection with as little as 10 PFU of HSV-1 strain F. By contrast, in the presence of passively administered neutralizing murine antibodies to HSV-1, some AR129 mice survived infection with up to104 PFU of HSV-1. This acute immune response was dependent on the presence of interleukin-12 (IL-12) p75. Interestingly, some virus-infected mice stayed healthy for several months, at which time antibody to HSV-1 was no longer detectable. Treatment of these virus-exposed mice with dexamethasone led to death in approximately 40% of the mice. HSV-1 was found in brains of mice that did not survive dexamethasone treatment, whereas HSV-1 was absent in those that survived the treatment. We conclude that in the presence of passively administered HSV-1-specific antibodies, the IL-12-induced IFN-gamma -dependent innate immune response is able to control low doses of virus infection. Surprisingly, in a significant proportion of these mice, HSV-1 appears to persist in the absence of antibodies and specific immunity.

* Corresponding author. Mailing address: Institute of Virology, University of Zurich, Winterthurerstr. 266a, CH-8057 Zurich, Switzerland. Phone: 41 1 635 87 17. Fax: 41 1 635 89 11. E-mail: msuter{at}vetvir.unizh.ch.

Journal of Virology, October 2001, p. 9596-9600, Vol. 75, No. 20
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.20.9596-9600.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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