NeuroAIDS

Contributions of the human immunodeficiency virus-1 proteins Tat and gp120 as well as CD40 to microglial activation

T. G. D'Aversa, Eliseo Eugenin, Joan W. Berman

Research output: Contribution to journalReview article

52 Citations (Scopus)

Abstract

Microglia are the resident phagocytes of the brain and are an important source of proinflammatory mediators. Human immunodeficiency virus (HIV)-1 infects the central nervous system early in the course of disease, and it is believed that this occurs, in part, through the transmigration of HIV-1-infected cells across the blood-brain barrier. Infected cells release viral proteins, such as Tat and gp120. After microglia interact with these proteins, they become activated and secrete chemokines; upregulate key surface receptors, such as CD40, and also activate resident cells. This review focuses on the consequences of microglial activation in NeuroAIDS, with an emphasis on chemokine production and CD40 upregulation after interaction with tat or gp120. The importance of microglial CD40 in two other neurological diseases, Alzheimer's disease and multiple sclerosis, is also discussed.

Original languageEnglish (US)
Pages (from-to)436-446
Number of pages11
JournalJournal of Neuroscience Research
Volume81
Issue number3
DOIs
StatePublished - Aug 1 2005
Externally publishedYes

Fingerprint

Microglia
Chemokines
HIV-1
Alzheimer Disease
Up-Regulation
Viral Proteins
Phagocytes
Blood-Brain Barrier
Multiple Sclerosis
Central Nervous System
Brain
Human immunodeficiency virus 1 gp120 protein
Proteins

Keywords

  • Alzheimer's disease
  • Chemokines
  • Migration
  • Multiple sclerosis
  • Neurotoxicity

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

NeuroAIDS : Contributions of the human immunodeficiency virus-1 proteins Tat and gp120 as well as CD40 to microglial activation. / D'Aversa, T. G.; Eugenin, Eliseo; Berman, Joan W.

In: Journal of Neuroscience Research, Vol. 81, No. 3, 01.08.2005, p. 436-446.

Research output: Contribution to journalReview article

@article{7af7c06b5e014ce8821f1f0fc00f896a,
title = "NeuroAIDS: Contributions of the human immunodeficiency virus-1 proteins Tat and gp120 as well as CD40 to microglial activation",
abstract = "Microglia are the resident phagocytes of the brain and are an important source of proinflammatory mediators. Human immunodeficiency virus (HIV)-1 infects the central nervous system early in the course of disease, and it is believed that this occurs, in part, through the transmigration of HIV-1-infected cells across the blood-brain barrier. Infected cells release viral proteins, such as Tat and gp120. After microglia interact with these proteins, they become activated and secrete chemokines; upregulate key surface receptors, such as CD40, and also activate resident cells. This review focuses on the consequences of microglial activation in NeuroAIDS, with an emphasis on chemokine production and CD40 upregulation after interaction with tat or gp120. The importance of microglial CD40 in two other neurological diseases, Alzheimer's disease and multiple sclerosis, is also discussed.",
keywords = "Alzheimer's disease, Chemokines, Migration, Multiple sclerosis, Neurotoxicity",
author = "D'Aversa, {T. G.} and Eliseo Eugenin and Berman, {Joan W.}",
year = "2005",
month = "8",
day = "1",
doi = "10.1002/jnr.20486",
language = "English (US)",
volume = "81",
pages = "436--446",
journal = "Journal of Neuroscience Research",
issn = "0360-4012",
publisher = "Wiley-Liss Inc.",
number = "3",

}

TY - JOUR

T1 - NeuroAIDS

T2 - Contributions of the human immunodeficiency virus-1 proteins Tat and gp120 as well as CD40 to microglial activation

AU - D'Aversa, T. G.

AU - Eugenin, Eliseo

AU - Berman, Joan W.

PY - 2005/8/1

Y1 - 2005/8/1

N2 - Microglia are the resident phagocytes of the brain and are an important source of proinflammatory mediators. Human immunodeficiency virus (HIV)-1 infects the central nervous system early in the course of disease, and it is believed that this occurs, in part, through the transmigration of HIV-1-infected cells across the blood-brain barrier. Infected cells release viral proteins, such as Tat and gp120. After microglia interact with these proteins, they become activated and secrete chemokines; upregulate key surface receptors, such as CD40, and also activate resident cells. This review focuses on the consequences of microglial activation in NeuroAIDS, with an emphasis on chemokine production and CD40 upregulation after interaction with tat or gp120. The importance of microglial CD40 in two other neurological diseases, Alzheimer's disease and multiple sclerosis, is also discussed.

AB - Microglia are the resident phagocytes of the brain and are an important source of proinflammatory mediators. Human immunodeficiency virus (HIV)-1 infects the central nervous system early in the course of disease, and it is believed that this occurs, in part, through the transmigration of HIV-1-infected cells across the blood-brain barrier. Infected cells release viral proteins, such as Tat and gp120. After microglia interact with these proteins, they become activated and secrete chemokines; upregulate key surface receptors, such as CD40, and also activate resident cells. This review focuses on the consequences of microglial activation in NeuroAIDS, with an emphasis on chemokine production and CD40 upregulation after interaction with tat or gp120. The importance of microglial CD40 in two other neurological diseases, Alzheimer's disease and multiple sclerosis, is also discussed.

KW - Alzheimer's disease

KW - Chemokines

KW - Migration

KW - Multiple sclerosis

KW - Neurotoxicity

UR - http://www.scopus.com/inward/record.url?scp=25444487187&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=25444487187&partnerID=8YFLogxK

U2 - 10.1002/jnr.20486

DO - 10.1002/jnr.20486

M3 - Review article

VL - 81

SP - 436

EP - 446

JO - Journal of Neuroscience Research

JF - Journal of Neuroscience Research

SN - 0360-4012

IS - 3

ER -