“…Besides the crucial role of innate immune cells to combat TBEV, there is evidence that some of these cells are infected by TBEV, favor viral spread or contribute to pathogenesis in TBEV infection. Some non-structural proteins of TBEV, such as NS1, NS2A, NS4A, NS4B or NS5, display antagonistic functions, thus, interfering with components of the innate immune response (reviewed in [ 3 , 69 , 70 , 71 , 72 ]; [ 73 ]). In addition, TBEV infection modulates expression patterns of many antiviral genes which are involved in the innate immune response such as genes for PRRs, cytokines or chemokines [ 74 ].…”