Journal of Virology, January 2001, p. 654-660, Vol. 75, No. 2
0022-538X/01/$04.00+0 DOI: 10.1128/JVI.75.2.654-660.2001
Laboratory of Persistent Viral Diseases, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana, 59840,1 and Institut für Virologie der Universität Würzburg, Würzburg, Germany2
Received 12 July 2000/Accepted 16 October 2000
The immunological resistance of a host to viral infections may be
strongly influenced by cytokines such as interleukin-12 (IL-12) and
gamma interferon (IFN-
), which promote T helper type 1 responses,
and IL-4, which promotes T helper type 2 responses. We studied the role
of these cytokines during primary and secondary immune responses
against Friend retrovirus infections in mice. IL-4- and IL-12-deficient
mice were comparable to wild-type B6 mice in the ability to control
acute and persistent Friend virus infections. In contrast, more than
one-third of the IFN-
-deficient mice were unable to maintain
long-term control of Friend virus and developed gross splenomegaly with
high virus loads. Immunization with a live attenuated vaccine virus
prior to challenge protected all three types of cytokine-deficient mice
from viremia and high levels of spleen virus despite the finding that
the vaccinated IFN-
-deficient mice were unable to class switch from
immunoglobulin M (IgM) to IgG virus-neutralizing antibodies. The
results indicate that IFN-
plays an important role during
primary immune responses against Friend virus but is dispensable during
vaccine-primed secondary responses.
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