Can Your Genes Predict MS Treatment Success? What the IL28B Study Tells Us
Multiple sclerosis (MS) is a complex immune-mediated disease that affects the central nervous system. While interferon-beta (IFNβ) is one of the most commonly prescribed therapies for relapsing–remitting MS, its effectiveness varies widely between individuals. Scientists have long been trying to understand why—could it be something in our genes?
Recent discoveries in hepatitis C treatment suggested that genetic variations in a gene called IL28B might influence how patients respond to interferon-based treatments. Could this same gene predict treatment success in MS? That’s exactly what a multinational team of researchers set out to investigate in a 2011 study.
What Is IL28B and Why Does It Matter?
The IL28B gene encodes for a type of interferon (IFN-λ3), a molecule involved in the body’s immune response to viral infections. Two specific variations (or polymorphisms)—known as rs8099917 and rs12979860—had already been linked to better outcomes with interferon-alpha treatment in people with hepatitis C.
Since interferon-alpha and interferon-beta are part of the same family and work through similar biological pathways, researchers wondered: could these same gene variants affect how people with MS respond to IFNβ therapy?
The Study: 588 Patients, 13 Centers, One Question
The researchers analyzed DNA from 588 people with MS who were treated with IFNβ. These patients were classified into two groups:
Responders: No disease progression or relapses after 2 years of treatment.
Non-responders: Experienced disease activity (relapses or worsening disability) during the same period.
Using cutting-edge genetic tools, the team tested each patient’s DNA for the two IL28B variants. The goal? To see if the presence of these polymorphisms was more common in either group.
The Results: A (Mostly) Clear Answer
The bottom line: There was no significant association between IL28B gene variants and how patients responded to IFNβ overall.
In other words, having the “good” version of IL28B (which helps hepatitis C patients) did not make MS patients more likely to benefit from interferon-beta.
There was one exception: a subgroup of patients from France showed a possible association between the gene and treatment response. But this result was borderline and needs to be replicated in further studies before any conclusions can be drawn.
Why This Matters (and Why It Doesn’t Solve Everything)
The results suggest that IL28B is not a useful genetic marker for predicting IFNβ treatment success in MS. While disappointing, this finding helps narrow the field—science often progresses as much through ruling things out as it does through new discoveries.
This study also underscores the complexity of MS. Unlike hepatitis C, which is directly caused by a virus, MS is likely driven by multiple factors—genetic, environmental, and perhaps even viral, though no single cause has been pinned down. That means a single gene like IL28B is unlikely to tell the whole story.
Takeaway: No Shortcuts in Personalized Medicine (Yet)
Despite the initial hope, IL28B isn’t the key to unlocking personalized treatment for MS—at least not when it comes to interferon-beta. Still, this study is a crucial step toward understanding which biological factors do influence treatment response. The quest for reliable genetic markers in MS continues, and future studies may identify other, more relevant genes.
Disclaimer: This blog post is based on the provided research article and is intended for informational purposes only. It is not intended to provide medical advice. Please consult with a healthcare professional for any health concerns.
References:
Malhotra et al. IL28B polymorphisms are not associated with the response to interferon-beta in multiple sclerosis, Journal of Neuroimmunology, 2011.
