Investigation of the effect of Equivac® HeV Hendra virus vaccination on Thoroughbred racing performance

Objective

To evaluate the effect of Equivac® HeV Hendra virus vaccine on Thoroughbred racing performance.

Design

Retrospective pre‐post intervention study.

Methods

Thoroughbreds with at least one start at one of six major south‐eastern Queensland race tracks between 1 July 2012 and 31 December 2016 and with starts in the 3‐month periods before and after Hendra virus vaccinations were identified. Piecewise linear mixed models compared the trends in ‘Timeform rating’ and ‘margin to winner’ before and after initial Hendra virus vaccination. Generalised linear mixed models similarly compared the odds of ‘winning’, ‘placing’ (1st–3rd) and ‘winning any prize money’. Timeform rating trends were also compared before and after the second and subsequent vaccinations.

Results

Analysis of data from 4208 race starts by 755 horses revealed no significant difference in performance in the 3 months before versus 3 months after initial Hendra vaccination for Timeform rating (P = 0.32), ‘Margin to winner’ (P = 0.45), prize money won (P = 0.25), wins (P = 0.64) or placings (P = 0.77). Further analysis for Timeform rating for 7844 race starts by 928 horses failed to identify any significant change in Timeform rating trends before versus after the second and subsequent vaccinations (P = 0.16) or any evidence of a cumulative effect for the number of vaccines received (P = 0.22).

Conclusion

No evidence of an effect of Hendra virus vaccination on racing performance was found. The findings allow owners, trainers, industry regulators and animal health authorities to make informed decisions about vaccination.     

LeuT-desipramine structure reveals how antidepressants block neurotransmitter reuptake

Tricyclic antidepressants exert their pharmacological effect-inhibiting the reuptake of serotonin, norepinephrine, and dopamine-by directly blocking neurotransmitter transporters (SERT, NET, and DAT, respectively) in the presynaptic membrane. The drug-binding site and the mechanism of this inhibition are poorly understood. We determined the crystal structure at 2.9 angstroms of the bacterial leucine transporter (LeuT), a homolog of SERT, NET, and DAT, in complex with leucine and the antidepressant desipramine. Desipramine binds at the inner end of the extracellular cavity of the transporter and is held in place by a hairpin loop and by a salt bridge. This binding site is separated from the leucine-binding site by the extracellular gate of the transporter. By directly locking the gate, desipramine prevents conformational changes and blocks substrate transport. Mutagenesis experiments on human SERT and DAT indicate that both the desipramine-binding site and its inhibition mechanism are probably conserved in the human neurotransmitter transporters.