3 Key Takeaways
Plain English Summary- 01Core Finding
A 37-year-old woman with multiple sclerosis on long-term rituximab developed rapidly progressive dementia.
- 02Study Evidence
Study design used a clinical case insight protocol to track clinical outcomes.
- 03Practical Meaning
Benefits and risks vary by individual health history — discuss with a healthcare professional.
What This Means for You
Potosi virus can cause fatal neuroinvasive disease in humans, as evidenced by convergent postmortem neuropathologic, molecular, and ultrastructural evidence. Chronic B-cell depletion may increase susceptibility to severe disease with arboviral infections, which may present without conventional CNS inflammatory markers. CSF metagenomic sequencing should be considered in immunocompromised patients with unexplained progressive neurologic decline.
The Discovery
To establish Potosi virus, a mosquito-borne member of the family Peribunyaviridae , as a neuroinvasive human pathogen. A 37-year-old woman with multiple sclerosis on long-term rituximab developed rapidly progressive dementia. Serial MRI demonstrated progressive generalized atrophy. CSF showed transient, minimal lymphocytic pleocytosis. Extensive infectious, autoimmune, and prion evaluations were unrevealing, but CSF metagenomic sequencing detected all 3 genome segments for Potosi virus. Postmortem examination revealed diffuse meningoencephalitis with T-cell-predominant leptomeningeal and perivascular inflammation. Molecular analyses confirmed multiple nucleotide sequences with >99+% concordance with a known Potosi strain, with widespread viral infection confirmed by immunohistochemistry demonstrating intracellular and extracellular viral antigen. Electron microscopy demonstrated particles of a size consistent with the Peribunyaviridae family. Metagenomic sequencing of RNA extracted from frozen brain tissue identified all 3 Potosi virus gene segments without other infectious entities. Findings were concordant across multiple laboratories and institutions.
How It Works, Simply
This neurology research focuses on inflammation · T cells · Immune response. Researchers evaluated it using a standard-of-care clinical practice · Clinical case insight at the clinical practice stage of medical research.
3 Key Takeaways
Clinical Takeaways- 01Core Finding
A 37-year-old woman with multiple sclerosis on long-term rituximab developed rapidly progressive dementia.
- 02Study Evidence
Study design used a clinical case insight protocol to track clinical outcomes.
- 03Practical Meaning
Benefits and risks vary by individual health history — discuss with a healthcare professional.
Biological Mechanism & Study Design
Study Design & Cohort
Clinical case insight
Standard-of-care clinical practice · Clinical case insight · Clinical Practice
Biological Pathway & Modality
Inflammation · T cells · Immune response
Intervention: Establishing Potosi Virus as a Human Pathogen: Fatal Neuroinvasive Disease in a
Experimental Findings & Endpoints
To establish Potosi virus, a mosquito-borne member of the family Peribunyaviridae , as a neuroinvasive human pathogen.
A 37-year-old woman with multiple sclerosis on long-term rituximab developed rapidly progressive dementia. Serial MRI demonstrated progressive generalized atrophy.
CSF showed transient, minimal lymphocytic pleocytosis. Extensive infectious, autoimmune, and prion evaluations were unrevealing, but CSF metagenomic sequencing detected all 3 genome segments for Potosi virus.
Postmortem examination revealed diffuse meningoencephalitis with T-cell-predominant leptomeningeal and perivascular inflammation. Molecular analyses confirmed multiple nucleotide sequences with >99+% concordance with a known Potosi strain, with widespread viral infection confirmed by immunohistochemistry demonstrating intracellular and extracellular viral antigen.
Electron microscopy demonstrated particles of a size consistent with the Peribunyaviridae family. Metagenomic sequencing of RNA extracted from frozen brain tissue identified all 3 Potosi virus gene segments without other infectious entities.
Findings were concordant across multiple laboratories and institutions.
Clinical Translation & Practice Context
Potosi virus can cause fatal neuroinvasive disease in humans, as evidenced by convergent postmortem neuropathologic, molecular, and ultrastructural evidence.
Chronic B-cell depletion may increase susceptibility to severe disease with arboviral infections, which may present without conventional CNS inflammatory markers. CSF metagenomic sequencing should be considered in immunocompromised patients with unexplained progressive neurologic decline.
The Bottom Line · Clinical Pearl
“Potosi virus can cause fatal neuroinvasive disease in humans, as evidenced by convergent postmortem neuropathologic, molecular, and ultrastructural evidence.”
Published in Neurology · Current Stage: Clinical Practice
