IFIH1

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IFIH1

A gene on chromosome 2q24.2 that encodes an RNA helicase which, through its ATP-dependent unwinding of RNA, may promote message degradation by specific RNases. It is thought to have roles in suppressing growth and involved in innate immune defence viruses.

Molecular pathology
Genetic variation in IFIH1 is associated with diabetes mellitus insulin-dependent type 19.
References in periodicals archive ?
Characterization and immune response expression of the Rig-I-like receptor mda5 in common carp Cyprinus carpio.
A genetic analysis revealed that she had a mutation in the IFIH1 gene that caused her body to make dysfunctional MDA5 proteins in cells in her respiratory tract.
MDA5 can be exploited as efficacious genetic adjuvant for DNA vaccination against lethal H5N1 influenza virus infection in chickens.
It was first observed in Drosophila that microbial recognition of the receptor toll resulted in the expression of AMPs.[47] Similar to Drosophila, human toll-like receptors are present at the surface of airway epithelial cells or located in membrane-enclosed compartments.[48] Moreover, other patter recognition receptors (PRRs), such as NOD-like receptors, MDA5, and RIG-1, are located in the cell cytosol.[49] Ligation of PRRs leads to activation of cellular signaling transduction pathways such as MAPK and NF-?B.[50] This subsequently leads to expression of AMPs that are not produced at baseline conditions or only at very low levels.
(2006) Differential roles of MDA5 and RIG-I helicases in the recognition of RNA viruses.
First, retinoic acid-inducible gene I (RIG-I) and melanoma differentiation-associated gene 5 (MDA5), widely expressed in various types of cells, such as myeloid dendritic cells (DC), macrophages, epithelial cells, and fibroblasts, detect intracellular ssRNAs and transcriptional intermediates of IAV [3, 4].
Two DExD/H-box RNA helicases, retinoic acid-inducible gene 1 (RIG-1) and melanoma differentiation-associated gene 5 (MDA5), recognize double-stranded RNA and activate downstream signaling cascades through adaptor MAVS (VISA) [4-6].
Interestingly, MDA5 knockout mice develop demyelination of the central nervous system after viral infection.[10] It is rare that patients with anti-MDA5-positive dermatomyositis present as demyelinating polyneuropathy.
When physicians conducted a genetic analysis, it revealed she had a mutation in the IFIH1 gene that led her body to produce dysfunctional MDA5 proteins, which are vital to the immune system.
While rare, the team found multiple variations in IFIH1 that could lead to less effective MDA5. Interestingly, most people with these variations lived normal lifespans and had healthy children, leading researchers to suspect that other genetic factors may have compensated for the abnormality, or that people experienced frequent HRV infections but did not report them.
(117) Zika virus infection of human fibroblasts increased the expression of TLR3, RIG-I, and MDA5 RNA.
The detection of cytoplasmic viral RNA [85] is accomplished by RLRs as DDX58 (the retinoic acid inducible gene-1) (RIG-I), a RNA helicase that recognizes viral RNA present within the cytoplasm and melanoma differentiation-associated protein 5 (MDA5) [86].