ArticleThe Journal of experimental medicine1992
Viral neuroinvasion and encephalitis induced by lipopolysaccharide and its mediators.
Article in The Journal of experimental medicine, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
31 citing papers in PubMed, 94 citations in OpenAlex.
- Polyamines as Gatekeepers of Virus Replication and Central Nervous System Homeostasis.Pathogens (Basel, Switzerland) · 2026Review
- The mutation of Japanese encephalitis virus envelope protein residue 389 attenuates viral neuroinvasiveness.Virology journal · 2024Article
- Article
- Article
- Formation of fibroblastic reticular network in the brain after infection with neurovirulent murine coronavirus.Neuropathology : official journal of the Japanese Society of Neuropathology · 2016Article
- IV and IP administration of rhodamine in visualization of WBC-BBB interactions in cerebral vessels.Microscopy research and technique · 2015Article
- Brain Invasion by Mouse Hepatitis Virus Depends on Impairment of Tight Junctions and Beta Interferon Production in Brain Microvascular Endothelial Cells.Journal of virology · 2015Article
- Differential replicative ability of clinical dengue virus isolates in an immunocompetent C57BL/6 mouse model.BMC microbiology · 2015Article
- Interferon-λ restricts West Nile virus neuroinvasion by tightening the blood-brain barrier.Science translational medicine · 2015Article
- Systemic lipopolysaccharide compromises the blood-labyrinth barrier and increases entry of serum fluorescein into the perilymph.Journal of the Association for Research in Otolaryngology : JARO · 2014Article
- Systemic lipopolysaccharide induces cochlear inflammation and exacerbates the synergistic ototoxicity of kanamycin and furosemide.Journal of the Association for Research in Otolaryngology : JARO · 2014Article
- Differential replication of pathogenic and nonpathogenic strains of West Nile virus within astrocytes.Journal of virology · 2013Article
- West Nile virus-induced disruption of the blood-brain barrier in mice is characterized by the degradation of the junctional complex proteins and increase in multiple matrix metalloproteinases.The Journal of general virology · 2012Article
- West Nile virus: immunity and pathogenesis.Viruses · 2011Review
- Matrix metalloproteinase 9 facilitates West Nile virus entry into the brain.Journal of virology · 2008Article
- Drak2 contributes to West Nile virus entry into the brain and lethal encephalitis.Journal of immunology (Baltimore, Md. : 1950) · 2008Article
- Tissue tropism and neuroinvasion of West Nile virus do not differ for two mouse strains with different survival rates.Virology · 2007Article
- Correlation between breakdown of the blood-brain barrier and disease outcome of viral encephalitis in mice.Antiviral research · 2007Article
- Polyamines play a critical role in the control of the innate immune response in the mouse central nervous system.The Journal of cell biology · 2003Article
- Manipulation of cell surface macromolecules by flaviviruses.Advances in virus research · 2003Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study was designed to test the effect of bacterial endotoxin on penetration of viruses into the central nervous system (CNS). As a model we used two neurovirulent viruses that lack neuroinvasive capacity: West Nile virus-25 (WN-25) and neuroadapted Sindbis virus (SVN). Administration of lipopolysaccharide (LPS, 100 micrograms/mouse) to CD-1 mice, followed by WN-25 inoculation resulted in 83% encephalitis and death, compared with less than 5% in controls. The results in SVN-inoculated CD-1 mice were quite similar. LPS-treated mice suffered 62% mortality compared with 6% in the nontreated group. No changes in viral neuroinvasiveness were demonstrated in viruses isolated from brains of encephalitic mice, suggesting that neuroinvasion is not due to a selection process for an invasive variant, but to direct penetration of the viruses through the blood-brain barrier (BBB). LPS did not induce WN-25 encephalitis in LPS-insensitive C3H/HeJ mice, compared with 100% neuroinvasion in C3H/HeB mice. Induction of neuroinvasion could be transferred to C3H/HeJ mice by transfusion with serum obtained from LPS-treated, LPS-responsive mice. Passive immunization of CD-1 mice with anti-mTNF antibodies before LPS administration did not prevent LPS-induced WN-25 encephalitis. Furthermore, neutralization of tumor necrosis factor activity in the serum of LPS-treated mice did not abolish its activity, and transfusion-associated encephalitis was observed after the administration of the neutralized serum with WN-25. We suggest that LPS can contribute to virus penetration from the blood into the CNS, a process which turns a mild viral infection into a severe lethal encephalitis. This effect is mediated by soluble factors, and is probably achieved by injury to cerebral microvascular endothelium and modulation of BBB permeability.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.