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An enzyme-linked immunosorbent assay (elisa) was developed for the measurement of antirotaviral antibody in sera and faeces from pigs and used to study the dynamics of antirotaviral antibody responses in three cohorts of pigs. Piglets acquired antirotaviral antibody by sucking their dams soon after birth. Antirotaviral antibodies of IgA and IgG classes were detected in both colostrum and milk of all sows tested but IgM class antibodies were not. The antibody levels in colostrum were eight to 32 times higher than those in milk which was collected 18 days post partum. The levels of antibody in piglets' sera were comparable to those in colostrum but declined quickly to low levels by one month old. Maternal antibody was also detected in the faeces of piglets up to 18 days old. Natural rotavirus infection occurred in each of these cohorts when the geometric mean ELISA titres of maternal antibody in their sera declined to 1/1600 (by days 21, 25 and 30 for cohorts 1, 2 and 3, respectively). However, a positive correlation was not obtained between the levels of antirotaviral antibody and protection in individual litters within each of the cohort groups. In each of the cohorts, rotavirus infection usually occurred in one or two piglets first and then spread to other piglets in the same cohort. It is therefore suggested that maternally derived antibody is protective against rotavirus infection in piglets only for the first one or two weeks. Following natural infection with rotavirus, increases in serum antibodies were detected in two of the three cohorts by 20 to 30 days after the average time of onset of faecal shedding of virus. Faecal antibody was not detected by the elisatest following natural infection. Faecal shedding of rotavirus was not detected during the 14 days following experimental challenge of four pigs at 66 days old. Two of the pigs, however, had rising antibody titres (four- and eightfold) detected by elisa.

Representational difference analysis (RDA) was used to compare gene expression in equine mononuclear cells either infected with equine herpesvirus-2 (EHV-2) or adsorbed with inactivated EHV-2. Seven clones identified in non-infected cells after three rounds of selective subtraction and enrichment for differentially expressed genes contained sequences homologous to equine monocyte chemoattractant protein 1 (MCP-1). This suggested thatEHV-2 may down-regulate MCP-1 transcription in infected cells. These findings correlate well with similar findings described for human cytomegalovirus and support the view that EHV-2 may have the ability to modify the chemokine environment of infected cells. This may constitute an important feature of EHV-2 biology, because such an ability has the potential to compromise host defence mechanisms and predispose to infection with other pathogens.