Additionally, our studies revealed that while productive infection was inhibited upon treatment with IFN, EHDV-TAU retained its cell killing potential of LNCaP cells engineered to express JAK1 (LNCaP-JAK1), when infection was carried out in presence of interleukin-6 (IL-6), an inflammatory cytokine and strong activator of cell autonomous immunity [167]. Here, IFNA1 is linked to infection.