Equine assisted therapy and learning

This study examines the practices of Equine Assisted Therapy and Learning in Australia. Among Equine Assisted Therapy (EAT) and Equine Assisted Learning (EAL) centers there is a large degree of variation in practice worldwide. The current study outlines a range of practices in two states in Australia where EAT and EAL have arisen and evolved from models developed elsewhere. The philosophical foundations, training and certification processes followed along with the types and training of horses involved are compared across facilities. The findings of the study illustrated the large variation in EAT and EAL in current practice in Australia. The results suggested that if the practices of EAT and EAL are to move out of the “fringe” of mental health and learning professional practice and into the mainstream, their theoretical underpinnings, certification and licensure procedures, and methodology of practice must become more clearly defined

Recurrent emergence of SARS-CoV-2 spike deletion H69/V70 and its role in the Alpha variant B.1.1.7

We report severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike ΔH69/V70 in multiple independent lineages, often occurring after acquisition of receptor binding motif replacements such as N439K and Y453F, known to increase binding affinity to the ACE2 receptor and confer antibody escape. In vitro, we show that, although ΔH69/V70 itself is not an antibody evasion mechanism, it increases infectivity associated with enhanced incorporation of cleaved spike into virions. ΔH69/V70 is able to partially rescue infectivity of spike proteins that have acquired N439K and Y453F escape mutations by increased spike incorporation. In addition, replacement of the H69 and V70 residues in the Alpha variant B.1.1.7 spike (where ΔH69/V70 occurs naturally) impairs spike incorporation and entry efficiency of the B.1.1.7 spike pseudotyped virus. Alpha variant B.1.1.7 spike mediates faster kinetics of cell-cell fusion than wild-type Wuhan-1 D614G, dependent on ΔH69/V70. Therefore, as ΔH69/V70 compensates for immune escape mutations that impair infectivity, continued surveillance for deletions with functional effects is warranted