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J Virol, April 1998, p. 2638-2646, Vol. 72, No. 4
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Immune Response to Mouse Mammary Tumor Virus in Mice Lacking the Alpha/Beta Interferon or the Gamma Interferon Receptor

Ivan Maillard,1 Pascal Launois,2,3,dagger Ioannis Xenarios,3 Jacques A. Louis,2,3 Hans Acha-Orbea,3,4 and Heidi Diggelmann1,*

Institute of Microbiology1 and Institute of Biochemistry,3 University of Lausanne, and World Health Organization Immunology Research and Training Center,2 Lausanne, and Ludwig Institute for Cancer Research, Lausanne Branch, Epalinges,4 Switzerland

Received 18 August 1997/Accepted 19 December 1997

Mouse mammary tumor virus (MMTV) is a retrovirus which induces a strong immune response and a dramatic increase in the number of infected cells through the expression of a superantigen (SAg). Many cytokines are likely to be involved in the interaction between MMTV and the immune system. In particular, alpha/beta interferon (IFN-alpha /beta ) and gamma interferon (IFN-gamma ) exert many antiviral and immunomodulatory activities and play a critical role in other viral infections. In this study, we have investigated the importance of interferons during MMTV infection by using mice with a disrupted IFN-alpha /beta or IFN-gamma receptor gene. We found that the SAg response to MMTV was not modified in IFN-alpha /beta R0/0 and IFN-gamma R0/0 mice. This was true both for the early expansion of B and T cells induced by the SAg and for the deletion of SAg-reactive cells at later stages of the infection. In addition, no increase in the amount of proviral DNA was detected in tissues of IFN-alpha /beta R0/0 and IFN-gamma R0/0 mice, suggesting that interferons are not essential antiviral defense mechanisms during MMTV infection. In contrast, IFN-gamma R0/0 mice had increased amounts of IL-4 mRNA and an altered usage of immunoglobulin isotypes with a reduced frequency of IgG2a- and IgG3-producing cells. This was associated with lower titers of virus-specific antibodies in serum early after infection, although efficient titers were reached later.

* Corresponding author. Mailing address: Institute of Microbiology, Rue du Bugnon 44, 1011 Lausanne, Switzerland. Phone: 41-21-3144096. Fax: 41-21-3144095. E-mail: heidi.diggelmann{at}chuv.hospvd.ch.

dagger Permanent address: Pasteur Institute, Paris, France.




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