Gene Name | IFIT2 |
HF Protein Name | Interferon-induced protein with tetratricopeptide repeats 2 |
HF Function | Shows antiviral effect mainly at the level of viral replication |
Uniprot ID | P09913 |
Protein Sequence | View Fasta Sequence |
NCBI Gene ID | 3433 |
Host Factor (HF) Name in Paper | Ifit2 |
Gene synonyms | CIG-42 G10P2 IFI54 ISG54 |
Ensemble Gene ID | ENSG00000119922 |
Ensemble Transcript | ENST00000371826;ENST00000638108 |
KEGG ID | Go to KEGG Database |
Gene Ontology ID(s) | GO:0003723, GO:0005737, GO:0005783, GO:0005829, GO:0008637, GO:0009615, GO:0032091, GO:0035457, GO:0043065, GO:0051607, GO:0060337, |
MINT ID | N.A. |
STRING | Click to see interaction map |
GWAS Analysis | Click to see gwas analysis |
OMIM ID | 147040 |
PANTHER ID | PTHR10271:SF4 |
PDB ID(s) | 4G1T, |
pfam ID | PF13181, |
Drug Bank ID | N.A., |
ChEMBL ID | N.A. |
Organism | Homo sapiens (Human) |
Virus Name | Rabies virus |
Virus Short Name | RABV |
Order | Mononegavirales |
Virus Family | Rhabdoviridae |
Virus Subfamily | N.A. |
Genus | Lyssavirus |
Species | Rabies lyssavirus |
Host | Human, mammals |
Cell Tropism | N.A. |
Associated Disease | Rabies fatal encephalitis |
Mode of Transmission | Zoonosis, animal bite |
VIPR DB link | https://www.viprbrc.org/brc/vipr_allSpecies_search.spg?method=SubmitForm&decorator=rhabdo |
ICTV DB link | https://talk.ictvonline.org/ictv-reports/ictv_9th_report/negative-sense-rna-viruses-2011/w/negrna_viruses/201/rhabdoviridae |
Virus Host DB link | N.A. |
Paper Title | Ifit2 Is a Restriction Factor in Rabies Virus Pathogenicity |
Author's Name | Benjamin M. Davis, Volker Fensterl, Tessa M. Lawrence, Andrew W. Hudacek, Ganes C. Sen, Matthias J. Schnell |
Journal Name | Journal Of Virology |
Pubmed ID | 28637751 |
Abstract | Understanding the interactions between rabies virus (RABV) and individual host cell proteins is critical for the development of targeted therapies. Here we report that interferon-induced protein with tetratricopeptide repeats 2 (Ifit2), an interferon-stimulated gene (ISG) with possible RNA-binding capacity, is an important restriction factor for rabies virus. When Ifit2 was depleted, RABV grew more quickly in mouse neuroblastoma cells in vitro This effect was replicated in vivo, where Ifit2 knockout mice displayed a dramatically more severe disease phenotype than wild-type mice after intranasal inoculation of RABV. This increase in pathogenicity correlated to an increase in RABV mRNA and live viral load in the brain, as well as to an accelerated spread to brain regions normally affected by this RABV model. These results suggest that Ifit2 exerts its antiviral effect mainly at the level of viral replication, as opposed to functioning as a mechanism that restricts viral entry/egress or transports RABV particles through axons.IMPORTANCE Rabies is a fatal zoonotic disease with a nearly 100% case fatality rate. Although there are effective vaccines for rabies, this disease still takes the lives of about 50,000 people each year. Victims tend to be children living in regions without comprehensive medical infrastructure who present to health care workers too late for postexposure prophylaxis. The protein discussed in our report, Ifit2, is found to be an important restriction factor for rabies virus, acting directly or indirectly against viral replication. A more nuanced understanding of this interaction may reveal a step of a pathway or site at which the system could be exploited for the development of a targeted therapy. |
Used Model | C57Bl6/J mice |
DOI | 10.1128/JVI.00889-17 |