The small plaque virus (SPV), derived from the Onderstepoort strain of canine distemper virus (CDV) does not cause a lethal encephalitis in weanling hamsters. When we immunosuppressed hamsters infected with this virus they developed an acute disease, similar to that produced by the large plaque virus (LPV). Passive transfer of maternal antibody from SPV infected mothers to their offspring was effective in preventing acute disease following LPV infection. Co-infection of animals with both LPV and SPV resulted in increased hamster survival, associated with high titres of serum antibody. Similarly, heat inactivated SPV, present during infection with LPV, increased the survival rate. Heat inactivated LPV did not inhibit acute disease, although hamsters had high titres of neutralizing antibody. A small number of animals developed a delayed or recurring paralysis after immunosuppression, exposure to maternal antibody or co-infection. It would appear that the neurovirulence of CDV for hamsters can be modified by altering the levels of circulating antibody early in infection.