Influenza A infection in human airways shaped by opposing cell-type binding and replication preferences
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Influenza A virus infection of the human airway is governed by two cell-type-specific forces that partly offset each other, according to a study published in Science Advances. Avian influenza viruses preferentially bind ciliated airway cells, which carry higher levels of apical α2,3-linked sialic acid, but once inside they replicate comparably across cell types. Human influenza viruses also favor binding to ciliated cells, even though α2,6-linked sialic acid is similarly abundant on both cell types; however, they achieve higher viral RNA and protein levels in secretory cells, owing to compatibility with ANP32 proteins and differing ANP32A/B expression. The net result is similar infection levels in ciliated and secretory cells. The mechanism was established in human airway models; how these dynamics play out in infection in vivo remains to be worked out.
Written by a model from the reports · updated 3 hours ago
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- Sci AdvOpposing cell-type preferences for binding and replication shape influenza A virus infection in human airways.
A study shows influenza A virus tropism in human airways is shaped by both cell-type-specific binding preferences and replication capacity. Avian viruses preferentially bind ciliated cells because of higher apical α2,3-linked sialic acid levels, but replicate at similar levels in both cell types. Human viruses also preferentially bind ciliated cells despite comparable α2,6-linked sialic acid abundance, yet show higher viral RNA and protein levels in secretory cells owing to ANP32 protein compatibility and differences in ANP32A/B expression, resulting in similar infection levels across both cell types.
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