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Cited by 254

The DOI matches its Crossref record; 48 of the 48 references it cites were found in a registry or an index.

West Nile virus infection modulates human brain microvascular endothelial cells tight junction proteins and cell adhesion molecules: Transmigration across the in vitro blood-brain barrier

Open access
Verma, Saguna, Lo, Yeung, Chapagain, Moti, Lum, Stephanie, Kumar, Mukesh, Gurjav, Ulziijargal, Luo, Haiyan, Nakatsuka, Austin, Nerurkar, Vivek R.·2009·Virology
DOI 10.1016/j.virol.2008.11.047
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Abstract

Neurological complications such as inflammation, failure of the blood-brain barrier (BBB), and neuronal death contribute to the mortality and morbidity associated with WNV-induced meningitis. Compromised BBB indicates the ability of the virus to gain entry into the CNS via the BBB, however, the underlying mechanisms, and the specific cell types associated with WNV-CNS trafficking are not well understood. Brain microvascular endothelial cells, main component of the BBB, represent a barrier to virus dissemination into the CNS and could play key role in WNV spread via hematogenous route. To investigate WNV entry into the CNS, we infected primary human brain microvascular endothelial (HBMVE) cells with the neurovirulent strain of WNV (NY99) and examined WNV replication kinetics together with the changes in the expressions of key tight junction proteins (TJP) and cell adhesion molecules (CAM). WNV infection of HBMVE cells was productive as analyzed by plaque assay and qRT-PCR, and did not induce cytopathic effect. Increased mRNA and protein expressions of TJP (claudin-1) and CAM (vascular cell adhesion molecule and E-selectin) were observed at days 2 and 3 after infection, respectively, which coincided with the peak in WNV replication. Further, using an in vitro BBB model comprised of HBMVE cells, we demonstrate that cell-free WNV can cross the BBB, without compromising the BBB integrity. These data suggest that infection of HBMVE cells can facilitate entry of cell-free virus into the CNS without disturbing the BBB, and increased CAM may assist in the trafficking of WNV-infected immune cells into the CNS, via ‘Trojan horse’ mechanism, thereby contributing to WNV dissemination in the CNS and associated pathology.

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Metadata

Authors
Verma, S., Lo, Y., Chapagain, M., Lum, S., Kumar, M., Gurjav, U., Luo, H., Nakatsuka, A., & Nerurkar, V. R.
Venue
Virology
Publisher
Elsevier BV
Published
2009-03
Volume
385
Issue
2
Pages
425-433
ISSN
0042-6822 (ISSN-L)
DOI
10.1016/j.virol.2008.11.047
OpenAlex
W2040073120
Cited by
254
References
48
FWCI
8.48
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: West Nile virus infection modulates human brain microvascular endothelial cells tight junction proteins and cell adhesion molecules: Transmigration across the in vitro blood-brain barrier. https://app.cochat.ai/papers/10.1016/j.virol.2008.11.047
The paper
Verma, S., Lo, Y., Chapagain, M., Lum, S., Kumar, M., Gurjav, U., Luo, H., Nakatsuka, A., & Nerurkar, V. R. (2009). West Nile virus infection modulates human brain microvascular endothelial cells tight junction proteins and cell adhesion molecules: Transmigration across the in vitro blood-brain barrier. Virology. https://doi.org/10.1016/j.virol.2008.11.047

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.