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Published on: September 12, 2016
Treatment of progressive multifocal leukoencephalopathy with interleukin 7
Karl B Alstadhaug1, Thérèse Croughs2, Stian Henriksen3
1Department of Neurology, Nordland Hospital Trust, Bodø, Norway2Department of Clinical Medicine, UiT The Arctic University of Tromsø, Tromsø, Norway.
Insights
Recombinant human interleukin-7 showed promise in treating progressive multifocal leukoencephalopathy (PML) in an immunocompromised patient. This case highlights a potential new therapy for PML and related conditions.
Area of Science:
- Neuroimmunology
- Viral Pathogenesis
- Immunotherapy
Background:
- Progressive multifocal leukoencephalopathy (PML) is a rare, often fatal, demyelinating disease caused by the JC virus.
- Limited treatment options exist for PML, particularly in patients with underlying immunodeficiency.
Observation:
- A patient with PML and idiopathic CD4+ T-cell lymphocytopenia received compassionate use of recombinant human interleukin-7 (rhIL-7).
- The patient experienced clinical improvement, MRI lesion regression, JC virus DNA clearance, and increased CD4+ T-cell counts post-treatment.
Findings:
- Recombinant human interleukin-7 therapy led to a significant, albeit temporary, immune reconstitution and viral load reduction.
- The patient's CD4+ T-cell count increased, suggesting a restored immune response against the JC virus.
Implications:
- This case provides a proof-of-concept for rhIL-7 as a potential treatment for PML in immunocompromised individuals.
- Further clinical studies are warranted to establish the safety and efficacy of rhIL-7 for PML and other JC virus-related central nervous system infections.
Importance:
No reliable treatment options are known for progressive multifocal leukoencephalopathy with underlying immunodeficiency. We describe successful compassionate use of recombinant human interleukin 7 in a patient with idiopathic CD4+ T-cell lymphocytopenia.
Observations:
After the diagnoses of progressive multifocal leukoencephalopathy and idiopathic CD4+ T-cell lymphocytopenia were established, a 61-year-old man was treated with recombinant human interleukin 7 on November 1, 2012. Except for an episode of epilepsia partialis continua on January 16, 2013, a gradual clinical improvement was observed until March. Abnormalities shown on magnetic resonance imaging regressed; JC virus DNA in plasma, likely originating from the brain based on sequencing data, cleared; and increases in peripheral CD4+ T cells and JC virus intrathecal antibodies were observed. One year after treatment, the CD4+ T-cell count returned to baseline and the clinical improvement waned, possibly due to the patient's complex epilepsy. On the latest evaluation on January 14, 2014, the patient's condition was unchanged, with no signs of ongoing central nervous system infection.
Conclusions And Relevance:
The present case argues strongly for proof of the treatment concept. However, deeper insight into the JC virus and its pathogenesis and the immune response during central nervous system infection as well as further clinical studies are needed before recombinant human interleukin 7 can be recommended for the treatment of other cases of immunodeficiency and progressive multifocal leukoencephalopathy.
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