| Virus Name | Lassa virus |
| Virus Short Name | LASV |
| Order | Unassigned |
| Virus Family | Arenaviridae |
| Virus Subfamily | N.A. |
| Genus | Mammarenavirus |
| Species | Lassa virus |
| Host | Rodents and human |
| Cell Tropism | N.A. |
| Associated Disease | Hemorrhagic fever |
| Mode of Transmission | Zoonosis, fomite |
| VIPR DB link | https://www.viprbrc.org/brc/vipr_allSpecies_search.spg?method=SubmitForm&decorator=arena |
| ICTV DB link | https://talk.ictvonline.org/ictv-reports/ictv_9th_report/negative-sense-rna-viruses-2011/w/negrna_viruses/203/arenaviridae |
| Virus Host DB link | N.A. |
| Paper Title | Transferrin receptor 1 is a cellular receptor for New World haemorrhagic fever arenaviruses |
| Author's Name | Hyeryun Choe, Stephanie Jemielity, Jonathan Abraham, Sheli R. Radoshitzky and Michael Farzan |
| Journal Name | Current Opinion Microbiology |
| Pubmed ID | 21807555 |
| Abstract | t least five New World arenaviruses cause severe human hemorrhagic fevers. These viruses are transmitted to humans through contact with their respective South American rodent hosts. Each uses human transferrin receptor 1 (TfR1) as its obligate receptor. Accidental similarities between human TfR1 and TfR1 orthologs of arenaviral host species enable zoonoses, whereas mice and rats are not infectable because they lack these TfR1 determinants of infection. All pathogenic New World arenaviruses bind to a common region of the apical domain of TfR1. The ability of a New World arenavirus to use human TfR1 is absolutely predictive of its ability to cause hemorrhagic fevers in humans. Nonpathogenic arenaviruses, closely related to hemorrhagic fever arenaviruses, cannot utilize human TfR1 but efficiently enter cells through TfR1 orthologs of their native rodent hosts. Mutagenesis studies suggest that minor changes in the entry glycoproteins of these nonpathogenic viruses may allow human transmission. TfR1 is upregulated as a result of iron sequestration during the acute-phase response to infection, and the severity of disease may result from amplification of viral replication during this response. |
| Used Model | Vero, CHO and NIH 3T3 cells |
| DOI | 10.1016/j.mib.2011.07.014 |
