This is the first USDA licensed equine WNV vaccine to utilise a severe challenge model that produces the same WNV disease observed under field conditions to obtain a label claim for prevention of viraemia and aid in the prevention of WNV disease and encephalitis with a duration of immunity of 12 months.

Two smooth and six rough strains of Salmonella typhimurium with progressively smaller amounts of sugar and protein in their outer membrane were tested for degree of virulence in normal and iron-injected mice and for ability to acquire iron in mammalian sera. The rate of mortality showed that bacterial virulence for mice was lowered with progressive decrease of outer-membrane sugar and protein. Iron injections increased the rate of mortality in mice infected either with smooth strains or with superficially rough strains but were without effect in mice infected with deep rough strains. In in vitro experiments, iron promoted with equal effectiveness the growth of all serum-exposed bacterial strains, whereas enterobactin (E) was much more effective in promoting the growth of smooth and superficial rough than in promoting that of deep rough strains. Various experiments showed that deep rough strains cannot grow in E-supplemented serum because they are not able to use the transferrin-iron-E complexes that E forms with transferrin-iron. This failure to use transferrin-iron-E complexes by deep rough strains was found to be due to the inability of these strains to adsorb iron-containing complexes to their outer membrane. Adsorption studies with chemically treated bacteria showed that the receptor of transferrin-iron-E or Eiron complexes is a protein of the outer membrane of bacterial cells.

These studies establish that this live attenuated Flavivirus chimera is safe to use for immunoprophylaxis against WNV disease in horses.

The ability of pseudorabies virus (PrV) to down-modulate expression of major histocompatibility complex class I antigens in murine and porcine cells was investigated. When quantified by flow cytometry, surface expression of class I Kk and Dk antigens on PrV-infected cells decreased by 60% or more. Down-modulation was associated with a decrease in total cellular class I antigens, indicating regulation at the transcriptional or posttranscriptional level. PrV did not suppress expression of transferrin receptor, suggesting a selective regulatory mechanism.

A monoclonal antibody specific for the gI glycoprotein of virulent pseudorabies virus was produced and used to affinity purify gI glycoprotein. The purified gI was used in an enzyme-linked immunosorbent assay (ELISA) that identified and differentiated field virus-exposed animals from animals vaccinated with gI-deleted virus. The gI ELISA was evaluated by comparing it with the virus neutralization test and with a standard ELISA which does not distinguish between vaccinated and naturally infected animals. Pigs vaccinated with a gI-deleted vaccine were seropositive by the virus neutralization or standard ELISA but were seronegative in the gI ELISA. Nonvaccinated and vaccinated animals were detected as seropositive in the gI ELISA only after exposure to gI-containing field virus. Exposed animals were detected as early as day 7 and for as long as 141 days after field virus exposure. As little as 102.7 PFU of field virus was sufficient to seroconvert negative animals in the gI ELISA. Pseudorabies virus-seronegative animals which received multiple doses of gI-deleted vaccine remained seronegative in the gI ELISA. The use of this test to monitor swine for pseudorabies virus infection would offer significant benefits towards eradication of the disease.