ArticleThe Journal of infectious diseases2026
Presence of Lassa Virus RNA in Cerebrospinal Fluid Indicating Neuroinvasive Lassa Fever in Pediatric Patients From Edo State, Nigeria.
Article in The Journal of infectious diseases, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Lassa Virus-A Persistent and Evolving Threat.Microorganisms · 2026Review
- Evidence for Neuroinvasive Lassa Virus Infection in Pediatric Patients: Initial Findings and Implications.The Journal of infectious diseases · 2026Article
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34 authors.
Funding
Abstract
backgroundNeurological complications of Lassa fever (LF) are associated with fatal outcome. In this study, we aimed to provide further evidence of Lassa virus (LASV) infection of the central nervous system (CNS) by assessing LASV in cerebrospinal fluid (CSF).
methodsWe retrospectively screened the database of the LF diagnostic unit at Irrua Specialist Teaching Hospital in Nigeria for patients with suspected or confirmed LF who underwent lumbar puncture as part of their routine clinical management due to CNS symptoms and had CSF samples tested by LASV reverse-transcription polymerase chain reaction (RT-PCR).
resultsRT-PCR results for CSF were available for 153 patients, all children. LF was confirmed in 49 of 153 (32%) patients, of whom 42 (86%) were LASV RNA positive in CSF. Of the 42 patients, 33 (79%) were LASV RNA positive in CSF and plasma, whereas 9 (21%) patients were positive in CSF only. The CSF-positive LF patients had a median age of 10.5 years. Sample pairs of CSF and plasma taken within a day of each other on admission were available for 26 patients, of whom 23 (88%) had higher LASV RNA concentration in CSF compared to plasma (cycle threshold, 28.2 vs 36.7, respectively; P < .00001).
conclusionsLASV is frequently detected in CSF of pediatric LF patients with neurological symptoms. The virus load in CSF is usually higher than in plasma, indicating a neuroinvasive infection with active virus replication in CNS. Our findings have implications for clinical management of LF patients and drug development for LF.
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