Related Experiment Video
Updated: Dec 7, 2025
Tumor Engraftment in a Xenograft Mouse Model of Human Mantle Cell Lymphoma
Published on: March 30, 2018
Progressive multifocal encephalopathy in a patient with non-Hodgkin follicular lymphoma
I Trociukas1,2, A E Zirnis3, L Beļajeva2
1August Kirchenstein Institute of Microbiology and Virology, Riga Stradins University, Riga LV-1067, Latvia.
Abstract:
Progressive multifocal leukoencephalopathy (PML) is a rare and often fatal demyelinating disease of the central nervous system caused by John Cunningham virus (JCV). We present a case report of patient with non-Hodgkin follicular lymphoma, who developed PML after hematopoietic stem cell transplantation and rituximab-bendamustine therapy. JCV DNA was proven both in peripheral blood and cerebrospinal fluid. Patient with 4 years history of follicular lymphoma presented with progressing weakness in the right arm and leg and postural instability. Magnetic resonance imaging scans showed bilateral hyperintense lesions in the cerebellum and centrum semiovale consistent with findings in PML. JCV DNA was detected in patient peripheral blood and cerebrospinal fluid by real time polymerase chain reaction assay in CERBA laboratory (France). Human herpes simplex 6 and 7 DNA were also detected in peripheral blood by PCR. Patients condition rapidly deteriorated with exitus letalis after 3 months and 2 weeks from onset of symptoms. This case draws attention to risk for developing PML in patients with long-standing hematological malignancies.
Insights
Progressive multifocal leukoencephalopathy (PML), a rare brain disease caused by John Cunningham virus (JCV), occurred in a follicular lymphoma patient post-transplant. This case highlights the risk of PML in patients with long-standing hematologic malignancies.
Area of Science:
- Neuroscience
- Immunology
- Oncology
Background:
- Progressive multifocal leukoencephalopathy (PML) is a rare, fatal demyelinating CNS disease caused by John Cunningham virus (JCV).
- Hematologic malignancies, such as non-Hodgkin follicular lymphoma, are associated with increased risk of opportunistic infections.
Observation:
- A patient with a 4-year history of follicular lymphoma developed PML after hematopoietic stem cell transplantation and rituximab-bendamustine therapy.
- Clinical presentation included progressive weakness and postural instability, with MRI revealing characteristic PML lesions in the cerebellum and centrum semiovale.
- JCV DNA was detected in both peripheral blood and cerebrospinal fluid via real-time PCR.
Findings:
- The case confirms JCV as the causative agent of PML in this immunocompromised patient.
- Co-detection of Human herpes simplex virus 6 and 7 DNA in peripheral blood warrants further investigation regarding potential co-infections or their role in disease pathogenesis.
- The patient's condition rapidly deteriorated, leading to death within 3.5 months of symptom onset.
Implications:
- This case underscores the critical need for vigilance regarding PML development in patients with long-standing hematologic malignancies, particularly after intensive treatments like stem cell transplantation.
- Early detection and understanding of risk factors are crucial for managing PML in immunocompromised populations.
- Further research into the interplay between hematologic malignancies, immunosuppressive therapies, and viral reactivation (JCV, HHV-6, HHV-7) is warranted.
