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Mitochondria-Eating Protein Regulates Cellular Pathogenesis and Replication of H1N1 Influenza Virus

  • Writer: Yogy Simanjuntak
    Yogy Simanjuntak
  • Jul 2
  • 1 min read
Confocal microscopy panels show Mitotracker (red), Lysotracker (red), and HA-SPATA18 (green) with merged nucleus (blue) of H1N1-infected cell.
Confocal images of subcellular distribution and localization of mitochondria and lysosome in H1N1-infected cell

Rapid replication of RNA viruses requires substantial cellular energy and effective mechanisms to evade cellular immunity. To meet these demands, many RNA viruses manipulate mitochondrial dynamics, including mitochondrial fragmentation and mitophagy. In the upcoming hypothesis, I propose a potential role for mitochondria-eating protein (MIEAP, also known as SPATA18), a novel regulator of non-canonical mitophagy, in the cellular pathogenesis and replication of H1N1 influenza virus. I will also present several unpublished in vitro findings that support this hypothesis—stay tuned!


Read the Full Hypothesis with Preliminary Finding Now!

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