Virus Details


VHFID5145

Host Factor Information

Gene Name IFI35
HF Protein Name Interferon-induced 35 kDa protein
HF Function Supports Vesicular Stomatitis Virus replication
Uniprot ID P80217
Protein Sequence View Fasta Sequence
NCBI Gene ID 3430
Host Factor (HF) Name in Paper IFI35
Gene synonyms IFP35
Ensemble Gene ID ENSG00000068079
Ensemble Transcript ENST00000415816 [P80217-1];ENST00000438323 [P80217-2]
KEGG ID Go to KEGG Database
Gene Ontology ID(s) GO:0005634, GO:0005829, GO:0060337,
MINT ID P80217
STRING Click to see interaction map
GWAS Analysis Click to see gwas analysis
OMIM ID 600735
PANTHER ID PTHR15225:SF1
PDB ID(s) N.A.,
pfam ID PF07334, PF07292,
Drug Bank ID N.A.,
ChEMBL ID N.A.
Organism Homo sapiens (Human)

Pathogen Information

Virus Name Vesicular stomatitis Indiana virus
Virus Short Name VSV
Order Mononegavirales
Virus Family Rhabdoviridae
Virus Subfamily N.A.
Genus Vesiculovirus
Species Indiana vesiculovirus
Host Human, cattle, horse, swine, sandflies, blackflies
Cell Tropism N.A.
Associated Disease Vesicular diseases, encephalitis
Mode of Transmission Mostely by sandflies
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.

Publication Information

Paper Title Interferon-inducible protein IFI35 negatively regulates RIG-I antiviral signaling and supports vesicular stomatitis virus replication
Author's Name Anshuman Das, Phat X. Dinh, Debasis Panda, Asit K. Pattnaik
Journal Name Journal Of Virology
Pubmed ID 24371060
Abstract In a genome-wide small interfering RNA (siRNA) screen, we recently identified the interferon (IFN)-inducible protein 35 (IFI35 also known as IFP35) as a factor required for vesicular stomatitis virus (VSV) infection. Studies reported here were conducted to further understand the role and requirement of IFI35 in VSV infection. Consistent with the siRNA screening data, we found that depletion of IFI35 led to reduced VSV replication at the level of viral gene expression. Although no direct interaction of IFI35 with the viral replication machinery was observed, we found that IFI35 negatively regulated the host innate immune response and rescued poly(I·C)-induced inhibition of VSV replication. Promoter-driven reporter gene assays demonstrated that IFI35 overexpression suppressed the activation of IFN-beta and ISG56 promoters, whereas its depletion had the opposite effect. Further investigation revealed that IFI35 specifically interacted with retinoic acid-inducible gene I (RIG-I) and negatively regulated its activation through mechanisms that included (i) suppression of dephosphorylation (activation) of RIG-I and (ii) proteasome-mediated degradation of RIG-I via K48-linked ubiquitination. Overall, the results presented here suggest a novel role for IFI35 in negative regulation of RIG-I-mediated antiviral signaling, which will have implications for diseases associated with excessive immune signaling.
Used Model HeLa and HEK293 cells
DOI 10.1128/JVI.03202-13