Arbovirus infections can cause delayed neurological disease-eg, the development of Kozhevnikov's epilepsy and other sequelae after tick borne and Japanes encephalitis virus infections. Neuropsychiatric disease oflate onset has been reported in former Far East prisoners-of-war (FEPOW), and we have speculated that arboviruses might be the cause.
We tested sera from 281 FEPOW for haemagglutination inhibiting (HI) antibodies to three alphavirus, seven flaviviruses, and Bunyamwera virus (of the bunyavirus group), these viruses being chosen as representative of those found in South East Asia. Clinica! information, including full psychiatric investigation, was available in many cases.
Antibodies were found to all test antigens (titres 10-320), the flavivirus antibodies being the most common. 47% of sera had antibodies to one or more antigens, 24% to four or more, and 3% had antibodies to eight or nine antigens (a realistic finding since these antibodies tend to react with abroad range of related antigens). 26 of 49 (53%) men who had been in camps near the Thai-Burma border had antibodies, compared with I7 of 63 (27%) who had been elsewhere (p<0.0I). These sera were collected 30-32 years after rapatriation and, although there have been anecdotal reports of long-term persistence of arbovirus antibodies after long absence from endemic zone, we believe this is the only study in which a substantial number of non-immune subjects, known to have been exposed to infection over a limited period and then removed from possible reinfection, have been tested for persisting antibodies more than 30 years later. Such persistence of antibody must be due to persisting presence of antigen in some form; arboviruses are neurotropic and such persistence could be a hazard, particularly if reactivation occurred (as in the case of latent viruses such as herpes simplex).