Knowns and unknowns of TiLV-associated neuronal disease

ABSTRACT

Tilapia Lake Virus (TiLV) is associated with pathological changes in the brain of infected fish, but the mechanisms driving the virus’s neuropathogenesis remain poorly characterized. TiLV establishes a persistent infection in the brain of infected fish even when the virus is no longer detectable in the peripheral organs, rendering therapeutic interventions and disease management challenging. Moreover, the persistence of the virus in the brain may pose a risk for viral reinfection and spread and contribute to ongoing tissue damage and neuroinflammatory processes. In this review, we explore TiLV-associated neurological disease. We discuss the possible mechanism(s) used by TiLV to enter the central nervous system (CNS) and examine TiLV-induced neuroinflammation and brain immune responses. Lastly, we discuss future research questions and knowledge gaps to be addressed to significantly advance this field.

GRAPHICAL ABSTRACT

KEYWORDS:

• Tilapia lake virus
• fish nervous system
• neurotropic viral infection
• neurotropism
• neuroinflammation
• neuropathogenesis

Acknowledgements

We sincerely thank Dr. John Readman (Department of Infection, Immunity & Inflammation, GOS Institute of Child Health (ICH), University College London) for his wonderful assistance in the conceptualization of the images of the present manuscript.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Data Availability statement

Data sharing does not apply to this article, as no new data were generated or analyzed in this study.

Author contributions

J.E.K.R., F.N.H., D.S., K.D.T., W.S., K.R., J.M.D., N.G., and M.A. contributed to the conception and design; J.E.K.R. and F.N.H. drafted the initial version of the manuscript, J.E.K.R., F.N.H., D.S., K.D.T., W.S., K.R., J.M.D., N.G., and M.A. revised the manuscript critically for intellectual content; All Authors approved the final version of the manuscript; All Authors agree to be accountable for all aspects of the work.

Additional information

Funding

Mikolaj Adamek was supported by Deutsche Forschungsgemeinschaft (DFG project number 426513195). Krzysztof Rakus was supported by the National Science Centre of Poland under the Beethoven Life 1 project (grant number UMO-2018/31/F/NZ6/02311). This Open Access publication was funded by the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) - 491094227 “Open Access Publication Funding” and the University of Veterinary Medicine Hannover, Foundation.