Baculoviruses manipulate infected insects to climb to elevated positions before death, enhancing viral spread through a newly discovered molecular mechanism. The viruses hijack tachykinin, a neuropeptide produced in the host's midgut, to control phototactic climbing behavior. This behavioral manipulation ensures infected insects die at heights where viral particles can disperse more effectively to new hosts. The research reveals how the virus co-opts the host's own signaling molecules to alter neural pathways controlling movement and light-seeking behavior. By commandeering midgut-derived tachykinin, the pathogen essentially rewires the insect's behavioral circuitry to serve viral transmission needs. This represents a sophisticated example of parasitic manipulation, where the virus has evolved to exploit host neurochemical systems for its reproductive advantage. The findings illuminate the molecular basis of how pathogens can alter complex behaviors in their hosts, demonstrating the intricate evolutionary arms race between viruses and their targets. Understanding these mechanisms could inform strategies for controlling viral outbreaks in insect populations and provide insights into host-pathogen interactions more broadly.