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Journal of Virology, May 2008, p. 4931-4937, Vol. 82, No. 10
0022-538X/08/$08.00+0 doi:10.1128/JVI.02127-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Immunology and Virology Program, Centre for Ophthalmology and Visual Science, The University of Western Australia, Western Australia, Australia,1 Centre for Experimental Immunology, Lions Eye Institute, Nedlands, Western Australia, Australia,2 Cancer Immunology Program, Sir Donald and Lady Trescowthick Laboratories, Peter MacCallum Cancer Centre, East Melbourne 3002, Victoria, Australia3
Received 27 September 2007/ Accepted 6 February 2008
Both innate and adaptive immune responses participate in the control of murine cytomegalovirus (mCMV) infection. In some mouse strains, like BALB/c, the control of infection relies on the activities of CD8+ T cells. mCMV-specific CD8+ T-cell responses are unusual in that, even after mCMV has been controlled in the periphery, the numbers of circulating virus-specific CD8+ T cells remain high compared to those observed in other viral infections. To better understand the generation and maintenance of mCMV-specific CD8+ T-cell responses, we evaluated how antigen load and effector molecules, such as perforin (Prf) and gamma interferon (IFN-
), influence these responses during acute infection in vivo. Viral burden affected the magnitude, but not the early kinetics, of antigen-specific CD8+ T-cell responses. Similarly, the magnitude of virus-specific CD8+ T-cell expansion was affected by Prf and IFN-
, but contraction of antigen-specific responses occurred normally in both Prf- and IFN-
-deficient mice. These data indicate that control of mCMV-specific CD8+ T-cell expansion and contraction is more complex than anticipated and, despite the role of Prf or IFN-
in controlling viral replication, a full program of T-cell expansion and contraction can occur in their absence.
Published ahead of print on 12 March 2008.
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