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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.

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Journal ArticleDOI

Neuroinflammation During RNA Viral Infections

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.
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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.
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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.

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.
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Virus entry and replication in the brain precedes blood-brain barrier disruption during intranasal alphavirus infection.

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.