Equine herpes virus 1 causes respiratory infection in equine world-wide. Virus replicates in the respiratory tissues in ciliated and non-ciliated epithelial cells lining the nasal turbinate bones, trachea, bronchi, bronchioles, and type I and type II pneumocytes, and becomes viraemic causing myeloencephalopathy (paresis) and retinopathy. The virus later becomes latent. While active the virus crosses the placenta and leads to abortion of dead or dying foetuses and neonatal death. Infected horses show transient immunity after natural or experimental infection and immune responses to EHV-1 begin to decline after a few months of infection. Due to the transient nature of the immune response, horses are prone to subsequent reinfection and as a result development of an effective vaccine continues to be a challenge till to date.
In order to discover the role of neutralizing antibodies in the pathogenesis of EHV-1 infection, we studied the role of neutralizing antibodies in a murine model of infection during the acute stage of infection by passively immunizing mice by the subcutaneous route with a pre-immune or hyperimmune polyclonal rabbit neutralizing serum 24 hours before virus infection. Mice were challenged intranasally with live EHV-1 virus and virus replication in the respiratory tissues was studied on day 3 and 5 post infection (p.i., acute stage of infection). The effect of passive immunization was also studied on viraemia by infectious centers assays from buffy coat cells. Slight reduction in virus titres in the respiratory tissues and level of viraemia was noted on day 3 p.i, but this difference was not significant. However significant reduction was seen in virus titres both in respiratory tissues and on the state of viraemia on day 5 in passively immunized animals compared with the controls given pre-immune sera from the same rabbit. The sera of passively transferred mice were also tested for presence of rabbit neutralizing antibodies on day 3 and 5 (days 4 and 6) of antibody transfer, suggesting that for complete protection neutralizing IgA may be required at the mucosal surface to stop or otherwise inhibit the viral attachment and thereby explain the differences in viral titres. These results of antibody transfer at an acute stage of infection will be discussed in this communication.