H
Hamid Salimi
Researcher at Washington University in St. Louis
Publications - 12
Citations - 507
Hamid Salimi is an academic researcher from Washington University in St. Louis. The author has contributed to research in topics: Viral entry & Viral replication. The author has an hindex of 10, co-authored 12 publications receiving 326 citations. Previous affiliations of Hamid Salimi include Roy J. and Lucille A. Carver College of Medicine & Burnet Institute.
Papers
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Journal ArticleDOI
Neuroinflammation During RNA Viral Infections
Robyn S. Klein,Charise Garber,Kristen E. Funk,Hamid Salimi,Allison Soung,Marlene Kanmogne,Sindhu Manivasagam,Shannon Agner,Matthew D. Cain +8 more
TL;DR: Mechanisms of RNA virus clearance and neurotoxicity during viral encephalitis are discussed with a focus on the cytokines essential for immune and neural cell inflammatory responses and interactions.
Journal ArticleDOI
Encephalitic Arboviruses: Emergence, Clinical Presentation, and Neuropathogenesis.
TL;DR: The major families of emerging arboviruses that cause neurologic infections, their neuropathogenesis and host neuroimmunologic responses, and current strategies for treatment and prevention of neurologic infection they cause are reviewed.
Journal ArticleDOI
Mechanisms of Pathogen Invasion into the Central Nervous System
TL;DR: Advances in understanding of the CNS invasion mechanisms of different neurotropic pathogens may enable the development of strategies to control their entry and deliver drugs to mitigate established infections.
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HIV-1 entry and trans-infection of astrocytes involves CD81 vesicles.
Lachlan Robert Gray,Stuart Turville,Tina L. Hitchen,Wan Jung Cheng,Anne Ellett,Hamid Salimi,Michael Roche,Steven Lodewyk Wesselingh,Paul R Gorry,Melissa J Churchill +9 more
TL;DR: The ability of astrocytes to transfer virus, without de novo viral synthesis suggests they are capable of sequestering and protecting virus and thus, they could potentially facilitate viral dissemination in the CNS.
Journal ArticleDOI
Virus entry and replication in the brain precedes blood-brain barrier disruption during intranasal alphavirus infection.
Matthew D. Cain,Hamid Salimi,Yongfeng Gong,Lihua Yang,Samantha L. Hamilton,James R. Heffernan,Jianghui Hou,Mark J. Miller,Robyn S. Klein +8 more
TL;DR: It is demonstrated that Venezuelan equine encephalitis virus (VEEV) strain TC83-GFP, a GFP expressing, attenuated strain with a G3A mutation within the 5' UTR that is associated with increased sensitivity to type I interferons (IFNs), does not directly impact BBB permeability and that mononuclear and endothelial cell interactions may underlie BBB disruption during alphavirusEncephalitis.