More importantly, the direct and strong interaction of AaVA-1 with CD4 could be an interesting mechanism to explore in terms of impact on CD4+ T cells expression and viral infections, a mechanism employed by the tick protein Salp15 in suppressing human immune system and facilitating the infection of the Lyme disease-causing agent Borrelia burgdorferi bacterial infection [47]. The gene discussed is CD4; the disease is Lyme disease.