Activation of the RIG-I/MAVS Signaling Pathway during Human Adenovirus Type 3 Infection Impairs the Pro-Inflammatory Response Induced by Secondary Infection with .

The exacerbation of pneumonia in children with human adenovirus type 3 (HAdV-3E) is secondary to a () infection. The influence of host-pathogen interactions on disease progression remains unclear. It is important to note that infections following an HAdV-3E infection are frequently observed in clinical settings, yet the underlying susceptibility mechanisms are not fully understood. This study utilized an A549 cell model to investigate secondary infection with following an HAdV-3E infection. The findings suggest that HAdV-3E exacerbates the infection by intensifying lung epithelial cell damage. The results highlight the role of HAdV-3E in enhancing the interferon signaling pathway through (), resulting in the increased expression of interferon-stimulating factors like , , and . The increase in interferon-stimulating factors inhibits the NF-κB and MAPK/P38 pro-inflammatory signaling pathways. These findings reveal new mechanisms of action for HAdV-3E and in secondary infections, enhancing our comprehension of pathogenesis.