Abstract
The board is set, the pieces are moving: Modulation of New World arenavirus entry by host proteins.
Highlights
Pathogenic New World arenaviruses (NWAs) like JUNV and MACV use transferrin receptor 1 (TfR1) of humans as well as their rodent host species as entry receptors, which is likely why they can be transmitted from rodents into humans [11,12]
We showed that Ltype voltage-gated calcium channels (VGCC), hetero-multimeric protein complexes that regulate Ca2+ influx into cells, are the main entry receptors for NWAs when they cannot use TfR1 on target cells (e.g., JUNV and MACV infection of mouse cells); VGCCs contribute to infection of human cells by NWAs that efficiently use TfR1 [14,15]
Using Trim2 knockout mice, we demonstrated that tripartite motif protein 2 (TRIM2) limits NWA entry in a ubiquitin ligase- and interferon-independent fashion, constituting a unique intrinsic restriction factors (RFs) within the TRIM family
Summary
Arenaviruses are enveloped viruses with 2 ambisense genomic RNA molecules, whose entry into cells is mediated by the viral glycoprotein (GP), generated by proteolytic processing of the precursor GPC into the subunits GP1 (the receptor-binding domain), GP2 (the transmembrane fusion protein), and the stable signal peptide [1]. NWAs exploit a variety of attachment factors and entry receptors at the cell surface.
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