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Trabajo presentado en la 18th International Conference on Diseases of Fish and Shellfish, celebrada en Belfast, del 4 al 8 de septiembre de 2017, When infected by pathogens, endotherms and ectotherms can both increase their body temperature to limit the infection. Ectotherms do so by moving to warmer places, hence the term ¿behavioral fever¿. We studied the expression of behavioral fever by common carp infected by cyprinid herpesvirus 3 (CyHV-3) using multi-chamber tanks encompassing a 24°C-32°C gradient. We showed that carp maintained at 24°C all died from the infection, whereas those housed in multichamber tanks all survived as a consequence of their transient migration to the warmest compartment. As the expression of behavioral fever occurred only at an advanced stage of the disease, we hypothesized that the virus might delay this phenomenon in order to promote its replication. This hypothesis was proved correct, and the delay mechanism was found to rely on the expression of a soluble viral decoy receptor for Tnf¿ encoded by CyHV-3 ORF12. This conclusion relied on three complementary observations: (i) a CyHV3 ORF12 deleted recombinant induced an early onset of behavioral fever in comparison to wild-type CyHV-3; (ii) ORF12 expression product binds and neutralizes carp Tnf¿; and (iii) injection of anti-Tnf¿ neutralizing antibodies suppressed behavioral fever, and decreased fish survival in response to infection. This study provides a unique example of how viruses have evolved to alter host behavior to increase fitness. It demonstrates that behavioral fever in ectotherms and fever in endotherms are evolutionarily and functionally related through common cytokine mediators that originated more than 400 million years ago. Finally, this study stresses the importance of the environment in the hostpathogen- environment triad.