| Virus Name | Measles Virus |
| Virus Short Name | MeV |
| Order | Mononegavirales |
| Virus Family | Paramyxoviridae |
| Virus Subfamily | N.A. |
| Genus | Morbilivirus |
| Species | Measles morbillivirus |
| Host | Vertebrates |
| Cell Tropism | N.A. |
| Associated Disease | Fever, rash |
| Mode of Transmission | Sexual contact, blood, breast feeding |
| VIPR DB link | http://www.viprbrc.org/brc/vipr_allSpecies_search.do?method=SubmitForm&decorator=paramyxo |
| ICTV DB link | https://talk.ictvonline.org/ictv-reports/ictv_9th_report/negative-sense-rna-viruses-2011/w/negrna_viruses/199/paramyxoviridae |
| Virus Host DB link | http://www.genome.jp/virushostdb/view/?virus_lineage=Paramyxoviridae |
| Paper Title | Neurokinin-1 enables measles virus trans-synaptic spread in neurons |
| Author's Name | Nina Makhortova, Peter Askovich, Catherine E. Patterson, Lisa A. Gechman, Norma P. Gerard and Glenn F. Rall |
| Journal Name | Virology |
| Pubmed ID | 17434199 |
| Abstract | Measles virus (MV), a morbillivirus that remains a significant human pathogen, can infect the central nervous system, resulting in rare but often fatal diseases, such as subacute sclerosing panencephalitis. Previous work demonstrated that MV was transmitted trans-synaptically and that, while a cellular receptor for the hemagglutinin (H) protein was required for MV entry, it was dispensable for subsequent cell-to-cell spread. Here, we explored what role the other envelope protein, fusion (F), played in trans-synaptic transport. We made the following observations: (1) MV-F expression in infected neurons was similar to that seen in infected fibroblasts; (2) fusion inhibitory peptide (FIP), an inhibitor of MV fusion, prevented both infection and spread in primary neurons; (3) Substance P, a neurotransmitter with the same active site as FIP, also blocked neuronal MV spread; and (4) both genetic deletion and pharmacological inhibition of the Substance P receptor, neurokinin-1 (NK-1), reduced infection of susceptible mice. Together, these data implicate a role for NK-1 in MV CNS infection and spread, perhaps serving as an MV-F receptor or co-receptor on neurons. |
| Used Model | Vero cells |
| DOI | 10.1016/j.virol.2007.02.033 |
