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Phosphatidylinositol 4,5-Bisphosphate Mediates the Co-Distribution of Influenza A Hemagglutinin and Matrix Protein M1 at the Plasma Membrane. | LitMetric

AI Article Synopsis

  • The influenza A virus (IAV) features a surface protein called hemagglutinin (HA) that is crucial for the virus's ability to infect cells, with its density correlating to infectivity levels.
  • Research has shown that HA clusters at the cell membrane are essential for viral assembly and budding, and these clusters depend on a lipid called phosphatidylinositol 4,5-bisphosphate (PIP2).
  • A compound named cetylpyridinium chloride (CPC) can disrupt the clustering of both the IAV matrix protein (M1) and HA by interfering with their interaction with PIP2, suggesting a mechanism for how IAV assembles itself effectively in the host cell.

Article Abstract

The fully assembled influenza A virus (IAV) has on its surface the highest density of a single membrane protein found in nature-the glycoprotein hemagglutinin (HA) that mediates viral binding, entry, and assembly. HA clusters at the plasma membrane of infected cells, and the HA density (number of molecules per unit area) of these clusters correlates with the infectivity of the virus. Dense HA clusters are considered to mark the assembly site and ultimately lead to the budding of infectious IAV. The mechanism of spontaneous HA clustering, which occurs with or without other viral components, has not been elucidated. Using super-resolution fluorescence photoactivation localization microscopy (FPALM), we have previously shown that these HA clusters are interdependent on phosphatidylinositol 4,5-biphosphate (PIP2). Here, we show that the IAV matrix protein M1 co-clusters with PIP2, visualized using the pleckstrin homology domain. We find that cetylpyridinium chloride (CPC), which is a positively charged quaternary ammonium compound known for its antibacterial and antiviral properties at millimolar concentrations, disrupts M1 clustering and M1-PIP2 co-clustering at micromolar concentrations well below the critical micelle concentration (CMC). CPC also disrupts the co-clustering of M1 with HA at the plasma membrane, suggesting the role of host cell PIP2 clusters as scaffolds for gathering and concentrating M1 and HA to achieve their unusually high cluster densities in the IAV envelope.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9698905PMC
http://dx.doi.org/10.3390/v14112509DOI Listing

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