Host immunogenetics in tick-borne encephalitis virus infection-The CCR5 crossroad

The human Tick-borne encephalitis virus (TBEV) infection is a complex event encompassing factors derived from the virus itself, the vectors, the final host, and the environment as well. Classically, genetic traits stand out among the human factors that modify the susceptibility and progression of infectious diseases. However, and although this is a changing scenario, studies evaluating the genetic factors that affect the susceptibility specifically to TBEV infection and TBEV-related diseases are still scarce. There are already some interesting pieces of evidence showing that some genes and polymorphisms have a real impact on TBEV infection. Also, the inflammatory processes involving tick-human interactions began to be understood in greater detail. This review focuses on the immunogenetic and inflammatory aspects concerning tick-host interactions, TBEV infections, and tick-borne encephalitis. Of note, it has been described that polymorphisms in CD209, GSTM1, IL-10, IL-28B, MMP9, OAS2, OAS3, and TLR3 have a statistically significant impact on TBEV infection. Besides, CCR5, its ligands, and the CCR5 Delta 32 genetic variant seem to have a very important influence on the infection and its immune responses. Taking this information into consideration, a special discussion regarding the effects of CCR5 on TBEV infection and tick-borne encephalitis will be presented. Emerging topics (such as exosomes, evasins, and CCR5 blockers) involving immunological and inflammatory aspects of TBEV-human interactions will also be addressed. Lastly, the current picture of TBEV infection and the importance to address the TBEV-associated problems through the One Health perspective will be discussed.