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The use of a hemagglutination inhibition (HI) assay to assess humoral immune response to equine influenza virus (EIV) vaccines from various manufacturers administered to previously immunized adult horses was investigated. Subjects were allocated into one of 3 groups and vaccinated with various commercially available vaccines. Groups were subdivided into subjects that received 1 dose of a particular vaccine and those that received a second dose, 30 d later. Serum was collected at various times to assess antibody responses to contemporary EIV Florida sub-lineage strains. Statistical significance was set at P < 0.05 and all groups had a significant increase in antibody titers pre- and post-administration of the first dose. In contrast, there was no significant difference between day 30 titers and titers at subsequent time points, regardless of protocol. We concluded that administration of various commercial influenza vaccines containing a different sub-lineage clade stimulated equivalent HI antibody titers after 1 booster vaccination.

We validated 2 multiplex real-time PCR (rtPCR) assays based on single nucleotide polymorphisms (SNPs) of the hemagglutinin-1 ( HA1) gene of H3N8 equine influenza A virus (EIV) to determine clade affiliation of prototype and field isolates. Initial validation of the 2 multiplex rtPCR assays (SNP1 and SNP2) was performed using nucleic acid from 14 EIV Florida sublineage clade 1 and 2 prototype strains. We included in our study previously banked EIV rtPCR-positive nasal secretions from 341 horses collected across the United States in 2012-2017 to determine their clade affiliation. All 14 EIV prototype strains were identified correctly as either Florida sublineage clade 1 or clade 2 using the 2 SNP target positions. Of 341 EIV rtPCR-positive samples, 337 (98.8%) and 4 (1.2%) isolates were classified as belonging to clade 1 and 2 Florida sublineage EIV, respectively. All clade 1 Florida sublineage EIV strains were detected in domestic horses, three clade 2 Florida sublineage EIV strains originated from horses recently imported into the United States, and one clade 2 Florida sublineage EIV strain originated from a healthy horse recently vaccinated with a modified-live intranasal EIV vaccine containing the American lineage strain A/eq/Kentucky/1991. EIV Florida sublineage clade differentiation using a fast and reliable multiplex rtPCR platform will help monitor the introduction of clade 2 Florida sublineage EIV strains into North America via international transportation.

Background: Dexamethasone is routinely administered to horses but its effect on the antibody response to a commercial EIV/EHV vaccine is unclear. Hypothesis: Horses receiving dexamethasone will have lower postvaccination antibody levels against EIV and EHV‐1 than vaccinated controls. Animals: Fifty‐five healthy adult research horses. Methods: Randomized cohort study. Control (no vaccine, group 1), vaccination only (EIV/EHV‐1/EHV‐4, Prestige 2, Merck Animal Health, group 2), vaccination and concurrent single intravenous dose of dexamethasone (approximately.05 mg/kg, group 3), vaccination and 3 intravenous doses of dexamethasone at 24 hours intervals (group 4). Serum SAA levels were measured on day 1 and day 3. Antibody levels against EIV (hemagglutination inhibition assay, Kentucky 2014 antigen) and EHV‐1 (multiplex ELISA targeting total IgG and IgG 4/7) were measured on day 1 and day 30. Results: Significantly increased mean antibody titers after vaccination were only noted against EIV and only after the vaccination alone (n = 14, prevaccine mean [prvm] 166.9, SD 259.6, 95% CI 16.95‐316.8; postvaccine mean [povm] 249.1, SD 257.2, 95% confidence interval [CI] 100.6‐397.6, P =.02) and the single dose dexamethasone (n = 14, prvm 93.14, SD 72.2, CI 51.45‐134.8; povm 185.1, SD 118, CI 116.7‐253.6, P =.01), but not after multiple doses of dexamethasone (n = 14, prvm 194.3, SD 258.3, CI 45.16‐343.4; povm 240.0, SD 235.7, CI 103.9‐376.1, P >.05). Conclusion: The effect of dexamethasone on the postvaccine antibody response varies depending on the dosing frequency and the antigen‐specific antibody type. [ABSTRACT FROM AUTHOR]

The evolution of pandemic influenza A viruses, based on continuing dependence on the aquatic avian gene reservoir, is established. The relationship between the influenza viruses and their host aquatic birds, and how such interactions persisted was discussed. Several conclusions were made based on the phylogenetic analysis of influenza A virus RNA segments for the internal and spike proteins. Among these were the confirmation of a global pool for the influenza virus in aquatic birds and the evolution of host-specific lineages.