| Gene Name | N.A. |
| HF Protein Name | N.A. |
| HF Function | VP1 interacts with the GM1 and triggers vacuole formation |
| Uniprot ID | N.A. |
| Protein Sequence | View Fasta Sequence |
| NCBI Gene ID | N.A. |
| Host Factor (HF) Name in Paper | GM1 |
| Gene synonyms | N.A. |
| Ensemble Gene ID | N.A. |
| Ensemble Transcript | N.A. |
| KEGG ID | Go to KEGG Database |
| Gene Ontology ID(s) | N.A., |
| MINT ID | N.A. |
| STRING | Click to see interaction map |
| GWAS Analysis | Click to see gwas analysis |
| OMIM ID | N.A. |
| PANTHER ID | N.A. |
| PDB ID(s) | N.A., |
| pfam ID | N.A., |
| Drug Bank ID | N.A., |
| ChEMBL ID | N.A. |
| Organism | Homo sapiens (Human) |
| Virus Name | Simian Virus 40 |
| Virus Short Name | SV40 |
| Order | Unassigned |
| Virus Family | Polyomaviridae |
| Virus Subfamily | N.A. |
| Genus | Betapolyomavirus |
| Species | Simian virus 40 |
| Host | Mammals, human |
| Cell Tropism | N.A. |
| Associated Disease | N.A. |
| Mode of Transmission | N.A. |
| VIPR DB link | N.A. |
| ICTV DB link | https://talk.ictvonline.org/ictv-reports/ictv_9th_report/dsdna-viruses-2011/w/dsdna_viruses/129/polyomaviridae |
| Virus Host DB link | N.A. |
| Paper Title | Interaction between simian virus 40 major capsid protein VP1 and cell surface ganglioside GM1 triggers vacuole formation |
| Author's Name | Yong Luo,a Nasim Motamedi, Thomas G. Magaldi, Gretchen V. Gee, Walter J. Atwood, Daniel DiMaio |
| Journal Name | mBio (American Society For Microbiology) |
| Pubmed ID | 27006465 |
| Abstract | Simian virus 40 (SV40), a polyomavirus that has served as an important model to understand many aspects of biology, induces dramatic cytoplasmic vacuolization late during productive infection of monkey host cells. Although this activity led to the discovery of the virus in 1960, the mechanism of vacuolization is still not known. Pentamers of the major SV40 capsid protein VP1 bind to the ganglioside GM1, which serves as the cellular receptor for the virus. In this report, we show that binding of VP1 to cell surface GM1 plays a key role in SV40 infection-induced vacuolization. We previously showed that SV40 VP1 mutants defective for GM1 binding fail to induce vacuolization, even though they replicate efficiently. Here, we show that interfering with GM1-VP1 binding by knockdown of GM1 after infection is established abrogates vacuolization by wild-type SV40. Vacuole formation during permissive infection requires efficient virus release, and conditioned medium harvested late during SV40 infection rapidly induces vacuoles in a VP1- and GM1-dependent fashion. Furthermore, vacuolization can also be induced by a nonreplicating SV40 pseudovirus in a GM1-dependent manner, and a mutation in BK pseudovirus VP1 that generates GM1 binding confers vacuole-inducing activity. Vacuolization can also be triggered by purified pentamers of wild-type SV40 VP1, but not by GM1 binding-defective pentamers or by intracellular expression of VP1. These results demonstrate that SV40 infection-induced vacuolization is caused by the binding of released progeny viruses to GM1, thereby identifying the molecular trigger for the activity that led to the discovery of SV40. |
| Used Model | N.A. |
| DOI | 10.1128/mBio.00297-16 |
