AI Article Synopsis
- - Norovirus is a major cause of gastroenteritis globally, and its ability to infect cells is influenced by the arrangement of lipids in cell membranes, although this connection has not been fully explored.
- - Research shows that the protein TMEM30a, which is part of lipid flippases, is essential for the replication of murine norovirus (MNV) and helps the virus bind and enter host cells.
- - The study reveals that lipid asymmetry in cell membranes aids in MNV infection and persistence, challenging previous assumptions about cell markers, as certain lipids do not inhibit the virus but are instead linked to its successful entry.
Article Abstract
Norovirus, the leading cause of gastroenteritis worldwide, is a non-enveloped virus whose tropism is determined in part by the expression patterns of entry receptors. However, the contribution of cellular lipids to viral entry is not well understood. Here, we determined that the asymmetrical distribution of lipids within membrane bilayers is required for murine norovirus (MNV) replication. Specifically, TMEM30a, an essential subunit of lipid flippases, is required for MNV replication in vitro. Disruption of TMEM30a in mouse intestinal epithelial cells prevents persistent, enteric infection by MNV in vivo. Mechanistically, TMEM30a facilitates MNV binding and entry. Surprisingly, exoplasmic phosphatidylserine (PS), a typical marker of dying cells, does not inhibit MNV infection. Rather, TMEM30a maintains a lipid ordered state that impacts membrane fluidity that is necessary for the low affinity, high avidity binding of MNV to cells. Our data provides a new role for lipid asymmetry in promoting non-enveloped virus infection and norovirus persistence in vivo.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11580941 | PMC |
| http://dx.doi.org/10.1101/2024.11.06.622376 | DOI Listing |
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