Key result
CVB3-mediated mitophagy suppresses type I and III interferon pathways by disrupting MAVS-TBK1 interactions, thereby promoting viral replication.
Why the study?
CVB3 causes systemic inflammatory diseases and subverts host autophagy to support replication, but the role of mitophagy in viral replication and host responses was not fully characterized.
Population
Human neural progenitor cells, HeLa and H9C2 cardiomyocytes
Design
In vitro preclinical study
Authors
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May promote CVB3 replication via interferon suppression in models; leaves open mitophagy targeting for human viral myocarditis.
CVB3-mediated mitophagy suppresses host interferon pathways by promoting mitochondrial fragmentation and sequestration, thereby facilitating viral replication and providing a potential mechanism for CVB3-induced viral myocarditis.
Oh et al. (2021) studied Coxsackievirus B3 (CVB3) infection. CVB3 infection and mitophagy modulation (CCCP, PINK1 knockdown) vs. Mock infection and vehicle control was evaluated on Viral replication and interferon pathway activation. CVB3-mediated mitophagy suppresses type I and III interferon pathways by disrupting MAVS-TBK1 interactions, thereby promoting viral replication.
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