Newly Discovered Mysterious Human Gene VILMIR Found to Be Activated by Flu, COVID-19 and RSV Infections

Medical News: In a remarkable scientific breakthrough that could pave the way for new antiviral treatments, researchers have identified a previously unknown genetic element in the human body that appears to play a crucial role in how we respond to respiratory viral infections like influenza, COVID-19, and RSV. This novel genetic sequence, a long noncoding RNA dubbed VILMIR (Virus-Inducible LncRNA Modulator of Interferon Response), was found to be strongly activated in the presence of these viruses - and might serve as a key regulator of the body’s immune defenses.


Newly Discovered Mysterious Human Gene VILMIR Found to Be Activated by Flu, COVID-19
and RSV Infections

The research team behind this discovery hails from several renowned institutions including North Carolina State University, the University of California Santa Cruz, the University of Tennessee Health Science Center, the University of Milan, and the Gladstone Institutes. Their work provides fresh insights into the hidden parts of our genome and how they can influence health and disease in ways we are only beginning to understand.
 
Until recently, much of our DNA was dismissed as “junk,” but recent advances have revealed that these noncoding regions - including long noncoding RNAs (lncRNAs) - can have vital roles in regulating biological functions. This Medical News report sheds light on how one such RNA, VILMIR, becomes activated during infection and helps fine-tune the body's immune response by influencing interferon activity, a major player in antiviral defense.
 
A Hidden Gene That Lights Up During Infection
The researchers made their discovery by analyzing over 120 publicly available RNA-sequencing datasets from studies involving various strains of the influenza virus. They consistently observed that VILMIR was strongly upregulated in infected human respiratory epithelial cells. That is, its expression surged when the body was under attack by the flu.
 
But it didn’t stop there. The team also found similar activation of VILMIR in cells infected with SARS-CoV-2 (the virus responsible for COVID-19) and respiratory syncytial virus (RSV). Using a technique called RT-qPCR, they experimentally validated that VILMIR expression spikes dramatically after viral infection, peaking around 18 hours post-infection before gradually tapering off - likely due to the onset of cell death from the infection itself.
 
They further demonstrated that treatment with interferon-beta (IFN-β), a powerful immune signaling molecule, also triggered VILMIR activation. The response was dose-dependent and time-sensitive, meaning the more IFN-β administered and the longer the treatment, the higher the VILMIR expression.
 
VILMIR Is Found Across Immune Cell Types Too
In a separate set of experiments, the scientists analyzed single-cell RNA data from bronchoalveolar lavage fluid taken from COVID-19 patients. These samples, which contain a mix of epithelial and immune cells from the lungs, revealed that VI LMIR was activated across multiple immune cell types, including T cells, macrophages, dendritic cells, and even B cells. Notably, T cells and macrophages showed a statistically significant increase in VILMIR expression compared to healthy controls.
 
To confirm whether this was due to the interferon response, they treated T cells and monocytes in vitro with IFN-β. The result was a significant upregulation of VILMIR in both cell types, further supporting its role as an interferon-stimulated gene (ISG).
 
Silencing VILMIR Weakens the Body’s Defense
To better understand what VILMIR does, the team used a CRISPR interference technique to silence its expression in A549 epithelial cells. The result was telling: cells with VILMIR knockdown showed a noticeably weaker transcriptional response to IFN-β treatment. More than 2,300 genes showed altered expression in the absence of VILMIR, suggesting that this lncRNA plays a broad role in shaping the immune landscape during infection.
 
Though the individual gene changes were modest in magnitude, the sheer number of genes involved hints that VILMIR may act as a kind of immune tuning dial - modifying the strength of the host’s antiviral response to maintain a delicate balance between protection and inflammation.

Interestingly, when IFNAR1 - the receptor needed to trigger the interferon response - was knocked out in liver-derived cells, VILMIR activation was completely abolished. This showed conclusively that VILMIR is tightly regulated by the interferon system and is not activated independently.
 
Implications for Treatment and Future Research
The discovery of VILMIR adds to the growing body of evidence that noncoding RNAs, once thought to be biological filler, are in fact key players in our health. The researchers believe that targeting VILMIR or manipulating its expression could open up new therapeutic avenues for treating severe viral infections like COVID-19, influenza, and RSV.
 
While more research is needed to fully understand how VILMIR functions at the molecular level, its consistent presence in interferon responses and across diverse cell types make it a promising candidate for further investigation. It may eventually be used as a biomarker for infection severity or even as a target for drugs that aim to boost the body’s own defenses.
 
Final Thoughts
The study reveals how much more there is to learn about our own genome and its complex interactions with pathogens. Discoveries like VILMIR highlight the importance of looking beyond traditional protein-coding genes and exploring the mysterious regions of our DNA for answers to some of the most pressing health challenges of our time.
 
VILMIR may be just one of thousands of hidden genetic regulators waiting to be uncovered, but its link to our immune response during viral infections makes it one of the most intriguing yet. Scientists are hopeful that with further study, this unassuming lncRNA could become a powerful tool in our ongoing battle against respiratory viruses.
 
The study findings were published in the peer reviewed Journal of Virology.
https://journals.asm.org/doi/10.1128/jvi.00141-25
 
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