FAdV-4 infection induces selective mitochondrial autophagy

Abstract

Fowl adenovirus serotype 4 (FAdV-4) is an infectious pathogen that poses a significant threat to the poultry industry. It is widely disseminated globally and is characterized by high infection and mortality rates. Mitochondria, as multifunctional dual membrane-enclosed eukaryotic organelles, maintain cellular homeostasis through various mechanisms. However, how FAdV-4 infection alters mitochondrial dynamics has not been previously established. In this study, transmission electron microscopy and immunofluorescence techniques were used to confirm that FAdV-4 infection can significantly alter mitochondrial morphology, disrupt mitochondrial fusion-fission homeostasis, and promote changes in the spatial distribution of mitochondria, causing them to gather around the nucleus. This leads to increased contact and interaction with other organelles. Preliminary analyses of the mechanistic basis for FAdV-4-mediated disruption of mitochondrial homeostasis revealed that the virus can induce selective mitophagy via the classical PINK1/Parkin signaling pathway and promote its own replication, which was confirmed by Western blotting. The novel findings regarding the ability of FAdV-4 to regulate mitochondrial morphology and function discussed in this study represent an important step forward, providing a foundation for further efforts to explore the underlying pathogenic mechanisms and to develop adjuvant approaches to preventing or managing FAdV-4 infection.