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Journal of Virology, June 1999, p. 4748-4754, Vol. 73, No. 6
Institute of Virology1
and Institute of Experimental
Immunology,3 University of Zürich, CH-8057
Zürich, Switzerland, and Department of Vaccine
Technology and Immunology, Intervet Int. B. V., 5830 AA
Boxmer, The Netherlands2
Received 16 November 1998/Accepted 11 March 1999
The importance of each of the two interferon (IFN) systems in
impeding herpesvirus replication and in stimulating virus-specific lymphocytes to control an acute systemic infection is not completely understood. To further our knowledge, pseudorabies virus, attenuated by
deletion of the glycoprotein E gene to impair its neurovirulence and by
deletion of the thymidine kinase gene
(gE
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Role of the Individual Interferon Systems and Specific Immunity
in Mice in Controlling Systemic Dissemination of Attenuated
Pseudorabies Virus Infection
TK
PRV), was used to infect wild-type
129Sv/Ev and congenic mice with immune system-associated genetic
deficiencies. Mice with mature B and T lymphocytes but lacking either
one or both functional receptors for members of each of the two IFN
families were infected with gE
TK
PRV. At 3 and 7 but not 14 days after infection, replicating
gE
TK
PRV could be isolated only from livers
or spleens of mice lacking the receptors for both IFN families, and
these mice survived the infection. Therefore, functional IFN receptors
were not required to induce a protective immune response against an
acute infection with gE
TK
PRV. Furthermore,
PRV-specific antibodies of all immunoglobulin G isotypes were produced
in these mice. Mice without mature B and T lymphocytes and lacking
either one or both functional receptors for members of each of the two
IFN families were also infected with
gE
TK
PRV. Three days after infection,
replicating virus could be isolated only from mice lacking both mature
B and T lymphocytes and functional IFN receptors, and these mice were
not able to clear the virus. We present evidence that mice with an
intact gamma IFN system but without mature B and T cells were able to
prevent systemic dissemination of gE
TK
PRV.
*
Corresponding author. Mailing address: Institute of
Virology, University of Zürich, Winterthurerstr. 266a, CH-8057
Zürich, Switzerland. Phone: 41 1 635 8717. Fax: 41 1 635 8911. E-mail: msuter{at}vetvir.unizh.ch.
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