Abstract
As obligate intracellular parasites, viruses must traverse the host-cell plasma membrane to initiate infection. This presents a formidable barrier, which they have evolved diverse strategies to overcome. Common to all entry pathways, however, is a mechanism of specific attachment to cell-surface macromolecules or ‘receptors’. Receptor usage frequently defines viral tropism, and consequently, the evolutionary changes in receptor specificity can lead to emergence of new strains exhibiting altered pathogenicity or host range. Several classes of molecules are exploited as receptors by diverse groups of viruses, including, for example, sialic acid moieties and integrins. In particular, many cell-adhesion molecules that belong to the immunoglobulin-like superfamily of proteins (IgSF CAMs) have been identified as viral receptors. Structural analysis of the interactions between viruses and IgSF CAM receptors has not shown binding to specific features, implying that the Ig-like fold may not be key. Both proteinaceous and enveloped viruses exploit these proteins, however, suggesting convergent evolution of this trait. Their use is surprising given the usually occluded position of CAMs on the cell surface, such as at tight junctions. Nonetheless, the reason for their widespread involvement in virus entry most probably originates in their functional rather than structural characteristics.
Highlights
Viruses are infectious nucleic acids that have evolved efficient mechanisms for shuttling their genomes between the host cells that they depend upon for replication
The authors suggest that junctional adhesion molecule A (JAM-A) plays a crucial role in establishment of viraemia, either by facilitating infection of endothelial cells leading to release of virus from apical cell surfaces into the bloodstream or receptor-specific transcytosis of virus across endothelial cells
Many diverse groups of viruses bind to IgSF CAMs at the cell surface to mediate cell entry
Summary
Viruses are infectious nucleic acids that have evolved efficient mechanisms for shuttling their genomes between the host cells that they depend upon for replication. A key stage in the viral replication cycle is cell entry. All viruses must traverse the host-cell’s plasma membrane and in many cases a cell wall. For those viruses that infect animals, the first stage of this process is attachment to a cell-surface macromolecule, the viral receptor. As the first step in the infection process, viral attachment represents an attractive target for intervention. Receptor binding is frequently the trigger for conformational changes in the virion itself. These structural rearrangements are thought to initiate the uncoating process—the controlled, targeted release of the genome to the site of replication
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More From: Philosophical Transactions of the Royal Society B: Biological Sciences
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