MAPK pathway orchestrates gallid alphaherpesvirus 1 infection through the biphasic activation of MEK/ERK and p38 MAPK signaling

Herpesviruses, representing the most evolutionarily successful viruses, adeptly maintain a dynamic equilibrium with their hosts throughout virus-host interactions. This enables long-term coexistence and presents a formidable challenge for achieving complete clearance upon infection. Currently, there are no drugs or methods capable of curing herpesvirus infections in humans and animals. The simultaneous activation of multiple members of the MAPK superfamily is a common occurrence induced by various herpesviruses. However, the biological implications and underlying mechanisms of this concurrent activation across diverse MAPK superfamily members remain to be fully elucidated. Our study proffers preliminary insights into the molecular mechanisms by which the comprehensive activation of the MAPK signaling pathway maintains a nuanced balance in the interaction between gallid alphaherpesvirus and infected cells. The implications of this study could potentially extend to shedding light on the roles and mechanisms of the MAPK signaling pathway in other herpesvirus infections as well.