SLC35A2 gene product modulates paramyxovirus fusion events during infection.
Paramyxoviruses are significant human and animal pathogens that include mumps virus (MuV), Newcastle disease virus (NDV) and the murine parainfluenza virus Sendai (SeV). Despite their importance, few host factors implicated in paramyxovirus infection are known. Using a recombinant SeV expressing des...
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| Format: | Article |
| Language: | English |
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Public Library of Science (PLoS)
2025-01-01
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| Series: | PLoS Pathogens |
| Online Access: | https://doi.org/10.1371/journal.ppat.1012531 |
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| author | Yanling Yang Yuchen Wang Danielle E Campbell Heng-Wei Lee Wandy Beatty Leran Wang Megan Baldridge Carolina B López |
| author_facet | Yanling Yang Yuchen Wang Danielle E Campbell Heng-Wei Lee Wandy Beatty Leran Wang Megan Baldridge Carolina B López |
| author_sort | Yanling Yang |
| collection | DOAJ |
| description | Paramyxoviruses are significant human and animal pathogens that include mumps virus (MuV), Newcastle disease virus (NDV) and the murine parainfluenza virus Sendai (SeV). Despite their importance, few host factors implicated in paramyxovirus infection are known. Using a recombinant SeV expressing destabilized eGFP (rSeVCdseGFP) in a loss-of-function CRISPR screen, we identified the CMP-sialic acid transporter (CST) gene SLC35A1 and the UDP-galactose transporter (UGT) gene SLC35A2 as essential for paramyxovirus infection. As expected, SLC35A1 knockout (KO) cells showed drastic reduction in infections with SeV, NDV and MuV due to the lack of cell surface sialic acids receptors. However, SLC35A2 KO cells revealed unknown critical roles for this factor in virus-cell and cell-to-cell fusion events for the different paramyxoviruses. While UGT was essential for virus-cell fusion during SeV entry to the cell, it was not required for NDV or MuV entry. Importantly, UGT promoted the formation of syncytia during MuV infection, suggesting a role in cell-to-cell virus spread. Our findings demonstrate that paramyxoviruses can bind to or enter A549 cells in the absence of canonical galactose-bound sialic-acid decorations and show that UGT facilitates paramyxovirus fusion processes involved in entry and spread. |
| format | Article |
| id | doaj-art-ebc44d018e57415ea724532d2e54cfdb |
| institution | Kabale University |
| issn | 1553-7366 1553-7374 |
| language | English |
| publishDate | 2025-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS Pathogens |
| spelling | doaj-art-ebc44d018e57415ea724532d2e54cfdb2025-02-05T05:30:50ZengPublic Library of Science (PLoS)PLoS Pathogens1553-73661553-73742025-01-01211e101253110.1371/journal.ppat.1012531SLC35A2 gene product modulates paramyxovirus fusion events during infection.Yanling YangYuchen WangDanielle E CampbellHeng-Wei LeeWandy BeattyLeran WangMegan BaldridgeCarolina B LópezParamyxoviruses are significant human and animal pathogens that include mumps virus (MuV), Newcastle disease virus (NDV) and the murine parainfluenza virus Sendai (SeV). Despite their importance, few host factors implicated in paramyxovirus infection are known. Using a recombinant SeV expressing destabilized eGFP (rSeVCdseGFP) in a loss-of-function CRISPR screen, we identified the CMP-sialic acid transporter (CST) gene SLC35A1 and the UDP-galactose transporter (UGT) gene SLC35A2 as essential for paramyxovirus infection. As expected, SLC35A1 knockout (KO) cells showed drastic reduction in infections with SeV, NDV and MuV due to the lack of cell surface sialic acids receptors. However, SLC35A2 KO cells revealed unknown critical roles for this factor in virus-cell and cell-to-cell fusion events for the different paramyxoviruses. While UGT was essential for virus-cell fusion during SeV entry to the cell, it was not required for NDV or MuV entry. Importantly, UGT promoted the formation of syncytia during MuV infection, suggesting a role in cell-to-cell virus spread. Our findings demonstrate that paramyxoviruses can bind to or enter A549 cells in the absence of canonical galactose-bound sialic-acid decorations and show that UGT facilitates paramyxovirus fusion processes involved in entry and spread.https://doi.org/10.1371/journal.ppat.1012531 |
| spellingShingle | Yanling Yang Yuchen Wang Danielle E Campbell Heng-Wei Lee Wandy Beatty Leran Wang Megan Baldridge Carolina B López SLC35A2 gene product modulates paramyxovirus fusion events during infection. PLoS Pathogens |
| title | SLC35A2 gene product modulates paramyxovirus fusion events during infection. |
| title_full | SLC35A2 gene product modulates paramyxovirus fusion events during infection. |
| title_fullStr | SLC35A2 gene product modulates paramyxovirus fusion events during infection. |
| title_full_unstemmed | SLC35A2 gene product modulates paramyxovirus fusion events during infection. |
| title_short | SLC35A2 gene product modulates paramyxovirus fusion events during infection. |
| title_sort | slc35a2 gene product modulates paramyxovirus fusion events during infection |
| url | https://doi.org/10.1371/journal.ppat.1012531 |
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