Alterations of membrane curvature during influenza virus budding

P005
Alterations of membrane curvature during influenza
virus budding
Agnieszka Martyna and Jeremy S. Rossman
University of Kent, Canterbury, UK
While many of the interactions required for influenza virus
assembly have been determined, the molecular machinery
needed to complete the budding process has only recently been
elucidated. We have found a new role for the influenza virus
M2 protein in meditating virus budding, independent from its
previously determined ion channel activity. Investigation into the
role of the M2 protein showed that the protein possesses a well
conserved amphipathic helix that is capable of altering membrane
curvature in a cholesterol-dependent manner. In a reducedcholesterol environment such as would be found at the neck of
a budding virion, we see that M2 causes positive membrane
curvature and scission, a process that is dependent on the M2
amphipathic helix. Utilizing reverse genetics to recover influenza
virus containing a mutated amphipathic helix we see that the M2
amphipathic helix is necessary for membrane scission and for the
release of budding virions. Further results using SUPER Template
and virus-like particle systems show that additional viral proteins
are capable of modifying membrane curvature and function to
define and initiate the budding event whereas the M2 protein
mediates membrane scission and completes the budding process.