Q.12 Interferon-β is produced by
- (A) Bacteria infected cells
- (B) Virus infected cells
- (C) Both virus and bacteria infected cells
- (D) Fungi infected cells
Interferon-β (IFN-β), a type I interferon, is a key antiviral cytokine alerting neighboring cells to viral invasion. Produced rapidly by infected cells, it induces an antiviral state via JAK-STAT signaling. This article solves the MCQ for biotech students, confirming (B) Virus infected cells.
IFN-β Role in Innate Immunity
Virus infection triggers pattern recognition receptors (PRRs) like RIG-I, MDA5, and TLR3 in host cells. These detect viral dsRNA/ssRNA, activating IRF3/7 for IFN-β transcription. Secreted IFN-β binds IFNAR receptors, upregulating ISGs (e.g., PKR, OAS) to inhibit replication.
Correct Answer: (B) Virus infected cells
IFN-β is primarily produced by virus-infected cells (fibroblasts, epithelial cells) as an early response. Plasmacytoid DCs amplify it later via TLR7/9, but the direct trigger is viral nucleic acids.Explanation of All Options
Each option’s IFN-β induction:
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(A) Bacteria infected cells
Incorrect as primary source. Bacteria trigger IFN-I via bacterial DNA/flagellin (TLR9/STING), but IFN-α dominates over IFN-β; less potent response. -
(B) Virus infected cells
Correct. Canonical trigger—dsRNA analogs like poly(I:C) induce high IFN-β via IRF3 in most somatic cells. -
(C) Both virus and bacteria infected cells
Incorrect. Bacterial induction is weaker/specific (e.g., Listeria via cGAS-STING); viruses are the hallmark inducer. -
(D) Fungi infected cells
Incorrect. Fungal β-glucans trigger dectin-1/IL-1 pathways, favoring pro-inflammatory cytokines (TNF-α, IL-6) over IFN-β.
Option Primary Trigger IFN-β Production Level Key Pathway (A) Bacteria Bacterial DNA Low STING/TLR9 (B) Virus Viral RNA/DNA High RIG-I/TLR3 (C) Both Mixed Variable N/A (D) Fungi β-glucans Minimal Dectin-1 Applications in Biotechnology
Recombinant IFN-β treats MS (e.g., Avonex) and hepatitis. In research, use poly(I:C) to induce in cell lines for antiviral studies. For bioinformatics, BLAST IFN-β promoters to analyze PRR binding sites.
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