Hamsters inoculated with the TC-83 vaccine strain of Venezuelan encephalitis (VEE) virus were protected against a normally lethal challenge by virulent VEE virus, strain 68U201, inoculated 30 h after vaccination. Protection was correlated with significantly decreased levels of challenge virus in target tissues (spleen and bone marrow). Inhibition of challenge virus replication was correlated more closely with the interferon concentrations in spleen and bone marrow than with the vaccine virus infectivities in these tissues at the time of challenge. The induction of early defence mechanisms involves the efficient interaction of virus with the spleen; although this interaction is more efficient for TC-83 vaccine, virulent VEE viruses are sensitive to the induced protective mechanism. Interferon appears to be a mediator of this mechanism.


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