Abstract
After a delay of 2 to 10 weeks or longer, clinical encephalitis developed in 15 per cent of mice which were protected against the acute stage of Semliki Forest virus (SFV) infection by antiserum. Some of these mice had high titres of SFV in their brains together with lesions of acute encephalitis while the others had subacute lesions and no virus was detected. When brains of apparently healthy mice which had survived the acute stage of SFV infection were examined, 90 per cent appeared to be histologically normal, but residual lesions of encephalitis were found in most of the remainder. Although no virus was detected in the brains of apparently healthy mice which survived the acute stage, the development of delayed encephalitis appeared to be due to persistence of SFV from the original infection. Examination of the sera of mice treated with antiserum suggested that most failed to develop active immunity.
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