Abstract
Influenza virus particles span ~55-nm to ~30-µm in length, but the role of filamentous particles remains elusive. Filaments package at most a single genome, but display on their surfaces disproportionately more hemagglutinins (HAs). During cell entry, 3-5 neighboring HAs form a fusion cluster, delivering the genome across the endosomal membrane. Here we identify influenza filaments as viral persisters increasing the probability of fusion-cluster formation and cell entry under HA-directed selective pressure. When HA function is limited, filamentous particles fuse more rapidly and more efficiently than do spherical ones, but their infectious advantage derives from their enhanced fusion efficiency rather than from rate effects. Filaments are refractory to extreme HA inactivation, presenting a built-in reservoir of particles that can adapt to any condition limiting HA function.
One Sentence Summary Filamentous virus particles resist inhibition at the level of membrane fusion in the absence of genetic change.
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