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Acquired immunity of A/J mice to mouse hepatitis virus 3 infection: dependence on interferon- synthesis and macrophage sensitivity to interferon-

¹ Instituto Butantan, Laboratorio de Imunologia Viral, Sao Paulo, Brasil
² Max-Planck-Institut für Immunbiologie, Freiburg, Germany
and³ Universite de Strasbourg, Inserm U74, Laboratoire de Virologie, Strasbourg, France

Coronavirus-free A/J mice (A/J-), in contrast to those naturally infected with coronavirus (A/J+), were shown to be susceptible to experimental infection with our strain of mouse hepatitis virus 3 (MHV3). A/J- mice experimentally hyperimmunized with inactivated MHV3 (A/Ji) became resistant to challenge with this virus. BALB/c mice free of (BALB/c-) or naturally infected with (BALB/c+) coronavirus, or hyperimmunized with inactivated MHV3 (BALB/ci), were always fully susceptible. All susceptible mice developed an acute hepatitis with a high virus titre in the tissues. Resistance mice developed a mile disease in which the low virus titres detected in the tissues were cleared. After infection, interferon (IFN)- synthesis in A/J- mice was lower than that in A/J+ and A/Ji mice; IFN- synthesis was very high in BALB/c+ and BALB/ci mice, but low in BALB/c- mice. Studies of the anti-MHV3 effect induced in macrophages in vitro showed that only IFN--activated A/J mouse macrophages were able to restrict partially the growth of MHV3, regardless of whether the animals had been immunized. The effect occurred only when the cells were activated with IFN- before virus infection. The results indicate that the resistance of A/J mice to our strain of MHV3 is not natural but is acquired after immunization, and that the mechanism involved is dependent on T cell activity, IFN- production and the sensitivity of macrophages to IFN-.

Received 13 August 1990; accepted 26 February 1991.

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