IFIH1

Chr 2ADAR

interferon induced with helicase C domain 1

Also known as: AGS7, Hlcd, IDDM19, IMD95, MDA-5, MDA5, RLR-2, SGMRT1

IFIH1 encodes MDA5, an intracellular sensor that detects viral RNA and activates interferon-mediated antiviral immune responses. Mutations cause Aicardi-Goutières syndrome, immunodeficiency, and Singleton-Merten syndrome with both autosomal dominant and autosomal recessive inheritance patterns. The gene is extremely intolerant to loss-of-function variants (pLI near zero), indicating that complete loss of MDA5 function is typically incompatible with normal development.

OMIMResearchSummary from RefSeq, OMIM, UniProt
GOFmechanismAD/ARLOEUF 1.553 OMIM phenotypes
Clinical SummaryIFIH1
🧬
Gene-Disease Validity (ClinGen)
IFIH1-related type 1 interferonopathy · ADDefinitive

Definitive — sufficient evidence for diagnostic panels

Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
💊
Clinical Trials
4 active or recruiting trials — potential therapeutic options may be available

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.55LOEUF
pLI 0.000
Z-score -1.57
OE 1.25 (1.011.55)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
-0.79Z-score
OE missense 1.10 (1.021.17)
586 obs / 534.7 exp
Tolerant

Tolerant to missense variation

Observed / Expected Ratios
LoF OE1.25 (1.011.55)
00.351.4
Missense OE1.10 (1.021.17)
00.61.4
Synonymous OE1.12
01.21.6
LoF obs/exp: 59 / 47.3Missense obs/exp: 586 / 534.7Syn Z: -1.33
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
definitiveIFIH1-related Aicardi-Goutieres syndromeOTHERAD
strongIFIH1-related Singleton-Merten syndromeGOFAD
DN
0.6064th %ile
GOF
0.6052th %ile
LOF
0.3164th %ile

This gene has evidence for multiple mechanisms of pathogenicity (gain-of-function and loss-of-function). The Badonyi & Marsh model scores dominant-negative highest among its predictions, but genomic evidence (constraint, ClinVar variant spectrum, and literature) most strongly supports gain-of-function. Different variants in this gene may act through different mechanisms — interpret in context of the specific variant.

GOF1 literature citation
LOF1 literature citation

Note: In-silico variant effect predictors (SIFT, PolyPhen, REVEL, CADD) may underestimate pathogenicity of missense variants in genes with GOF or DN mechanisms. Consider functional evidence and clinical context.

Literature Evidence

GOFAutosomal dominant IFIH1 gain-of-function mutations cause Aicardi-Goutieres syndrome.PMID:25080300
LOFWe highlight unique findings and provide additional evidence that heterozygous loss of function of the IFIH1 gene increases susceptibility to recurrent fevers.PMID:33440462

Predictions from Badonyi M, Marsh JA. PLoS ONE. 2024;19(8):e0307312.

ClinVar Variant Classifications

0 submitted variants in ClinVar

Protein Context — Lollipop Plot

IFIH1 · protein map & ClinVar variants

Showing all ClinVar variants across the protein. Search a specific variant to highlight its position.

3D Protein StructureAlphaFold
Clinical Literature
Open Research Assistant →