The study investigates the coordinated inflammatory responses in Egyptian rousette bats (ERBs), the natural reservoir of Marburg virus (MARV), to understand how they control MARV infection. ERBs typically harbor MARV asymptomatically, likely due to a coadapted host-immunity pathogen relationship. Previous research showed that ERBs mount a disease-tolerant strategy, limiting pro-inflammatory gene induction to prevent immunopathology. However, the active host-resistant strategy that limits MARV burden remains unclear. The study hypothesized that localized inflammatory responses are essential for controlling MARV replication in ERBs. Using dexamethasone to attenuate pro-inflammatory responses, the researchers found that ERBs naturally generate coordinated pro-inflammatory responses at liver foci of infection, involving recruited mononuclear phagocytes and T cells, which proliferate with MARV-specificity. When pro-inflammatory responses are suppressed, ERBs exhibit increased MARV replication, oral/rectal shedding, and severe liver pathology, resembling MVD in humans. These findings suggest that ERBs balance immunoprotective tolerance with discrete MARV-resistant pro-inflammatory responses. Additionally, natural immunomodulatory stressors like food scarcity and habitat disruption may enhance viral shedding and transmission, increasing outbreak risk. The study provides insights into the complex relationship between ERB immunity and MARV infection, highlighting the importance of early inflammatory responses in maintaining viral control.The study investigates the coordinated inflammatory responses in Egyptian rousette bats (ERBs), the natural reservoir of Marburg virus (MARV), to understand how they control MARV infection. ERBs typically harbor MARV asymptomatically, likely due to a coadapted host-immunity pathogen relationship. Previous research showed that ERBs mount a disease-tolerant strategy, limiting pro-inflammatory gene induction to prevent immunopathology. However, the active host-resistant strategy that limits MARV burden remains unclear. The study hypothesized that localized inflammatory responses are essential for controlling MARV replication in ERBs. Using dexamethasone to attenuate pro-inflammatory responses, the researchers found that ERBs naturally generate coordinated pro-inflammatory responses at liver foci of infection, involving recruited mononuclear phagocytes and T cells, which proliferate with MARV-specificity. When pro-inflammatory responses are suppressed, ERBs exhibit increased MARV replication, oral/rectal shedding, and severe liver pathology, resembling MVD in humans. These findings suggest that ERBs balance immunoprotective tolerance with discrete MARV-resistant pro-inflammatory responses. Additionally, natural immunomodulatory stressors like food scarcity and habitat disruption may enhance viral shedding and transmission, increasing outbreak risk. The study provides insights into the complex relationship between ERB immunity and MARV infection, highlighting the importance of early inflammatory responses in maintaining viral control.