Target intelligence / Profile preview

Viral double-stranded RNA (dsRNA) (dsRNA)

Target
dsRNA
Molecular classification
Nucleic acid, Pathogen-associated molecular pattern (PAMP), Immune agonist ligand
01

Overview

Viral double-stranded RNA (dsRNA) is a critical molecular signature of viral infection, produced as a replication intermediate by RNA viruses or through bidirectional transcription in DNA viruses (Source: PubMed, PMID: 28288100). In mammalian cells, long dsRNA helices act as potent pathogen-associated molecular patterns (PAMPs) that are typically absent under normal physiological conditions (Source: NIH). These structures are sensed by specialized host receptors, primarily Melanoma Differentiation-Associated protein 5 (MDA5) in the cytoplasm and Toll-like receptor 3 (TLR3) in endosomes (Source: UniProt, Q9BYX4). Upon binding, these receptors trigger signaling cascades involving IRF3 and NF-κB, leading to the robust production of Type I interferons and the establishment of an antiviral state (Source: StatPearls). Additionally, dsRNA directly activates the pro-apoptotic protein kinase R (PKR) and the 2-5-oligoadenylate synthetase (OAS)/RNase L pathway to halt viral protein synthesis and degrade viral genomes (Source: Wikipedia). Therapeutic strategies often utilize synthetic dsRNA analogs like Poly(I:C) or Rintatolimod to bolster the innate immune response against viruses and tumors, though careful dosing is required to avoid excessive systemic inflammation (Source: ClinicalTrials.gov).

Other names
Double-stranded RNAViral dsRNAvdsRNALong dsRNAPathogen-associated molecular pattern RNA
02

Mechanism of action

Binding and activation of pattern recognition receptors (PRRs) such as MDA5 and TLR3, leading to the activation of IRF3 and NF-κB transcription factors and subsequent induction of Type I interferons (Source: PubMed, PMID: 17475884). It also directly activates Protein Kinase R (PKR), which phosphorylates eIF2α to inhibit protein synthesis, and the OAS/RNase L pathway, which degrades viral and cellular RNA (Source: NIH).

03

Biological functions

Innate immune activationViral replication intermediateInduction of apoptosisInhibition of protein translationRNA degradation
04

Disease associations

InfectionCancerInflammationAutoimmune disease
05

Safety considerations

Cytokine release syndrome (CRS)Systemic inflammatory response syndrome (SIRS)Autoimmunity due to cross-reactivity with endogenous RNAFlu-like symptoms and severe pyrexia
06

Interacting drugs

Polyinosinic-polycytidylic acid (Poly(I:C))

4 more in the full profile.

07

Biomarkers

Interferon-beta (IFN-β)OAS1Phosphorylated EIF2S1 (p-eIF2α)MX1ISG15

Beyond the preview

Go deeper on Viral double-stranded RNA (dsRNA) (dsRNA).

Explore the evidence, development activity, and competitive landscape with Gosset’s full data platform.

Drug pipeline

Full profile access

Explore the programs pursuing this target and their development progress.

  • Drug candidates
  • Developers
  • Development stage

Clinical trials

Full profile access

Follow the clinical studies evaluating therapies directed at this target.

  • Trial design
  • Status
  • Readouts

Competitive landscape

Full profile access

Compare approaches across drug candidates, modalities, and indications.

  • Programs
  • Modalities
  • Indications

Literature & evidence

Full profile access

Investigate the research and source evidence behind target biology and development.

  • Publications
  • Sources
  • Analysis

Patents

Full profile access

Explore patent activity around therapies and technologies addressing this target.

  • Patents
  • Assignees
  • Technologies

Research & analysis

Full profile access

Connect target biology, drug development, and emerging evidence in your research.

  • Biology
  • Development news
  • Analysis

Bring the full picture into focus.

See how Gosset can support your research on Viral double-stranded RNA (dsRNA) (dsRNA).

Explore the full profile

Gosset Free

Get started with Gosset.

Enter your work email and we’ll be in touch with next steps.

Work email preferred.

Book a call