Evidence map›Paper›PMID 19768553›Full record

ReviewJournal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology2009

CNS inflammation and macrophage/microglial biology associated with HIV-1 infection.

Anjana Yadav, Ronald G Collman

Open access · greenAbstract readReview
In one paragraph

Review in Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 135 papers.

0numbers the graph read from it
0cells of the map it votes in
135citing papers in PubMed
6.1field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

135 citing papers in PubMed, 197 citations in OpenAlex.

  1. Trial
  2. Neonatal intrahippocampal HIV-1 protein Tat(1-86) injection: neurobehavioral alterations in the absence of increased inflammatory cytokine activation.International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience · 2014
    Trial
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  14. Role of microglia in brain development after viral infection.Frontiers in cell and developmental biology · 2024
    Review
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  16. Article
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  19. Dopamine, Immunity, and Disease.Pharmacological reviews · 2023
    Review
  20. Article

75 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Anjana YadavDepartment of Medicine and Center for AIDS Research, University of Pennsylvania School of Medicine, 522 Johnson Pavilion, 36th & Hamilton Walk, Philadelphia, PA 19104, USA.
Ronald G Collman
University of Pennsylvania · US

Funding

Virus & Reservoirs CoreP30AI045008 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI DAVID S METZGER · 1999 to 2026
$78.6M
SCID HU MODEL FOR HIV INFECTION OF THE CNSP01NS027405 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI GONZALEZ-SCARANO, FRANCISCO · 1989 to 2007
$8.2M
HIV: gp120, Chemokine Receptors &Macrophage ActivationR01MH061139 · NIMH · UNIVERSITY OF PENNSYLVANIA · PI COLLMAN, RONALD G · 1999 to 2015
$5.2M
Molecular and Cellular Biology of HIV EncephalopathyP50NS027405 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI GONZALEZ-SCARANO, FRANCISCO · 2008 to 2009
$2.2M
NIAID NIH HHS AI 54008NIAID NIH HHS P30 AI045008NIMH NIH HHS MH 61139NIMH NIH HHS R01 MH061139NINDS NIH HHS NS 27405NINDS NIH HHS P01 NS027405NINDS NIH HHS P50 NS027405
6 · The paper itself

Abstract

Human immunodeficiency virus type 1 (HIV-1) infection of the central nervous system (CNS) can result in neurological dysfunction with devastating consequences in a significant proportion of individuals with acquired immune deficiency syndrome. HIV-1 does not infect neurons directly but induces damage indirectly through the accumulation of activated macrophage/microglia (M/M) cells, some of which are infected, that release neurotoxic mediators including both cellular activation products and viral proteins. One mechanism for the accumulation of activated M/M involves the development in infected individuals of an activated peripheral blood monocyte population that traffics through the blood-brain barrier, a process that also serves to carry virus into CNS and establish local infection. A second mechanism involves the release by infected and activated M/M in the CNS of chemotactic mediators that recruit additional monocytes from the periphery. These activated M/M, some of which are infected, release a number of cytokines and small molecule mediators as well as viral proteins that act on bystander cells and in turn activate them, thus amplifying the cascade. These viral proteins and cellular products have neurotoxic properties as well, both directly and through induction of astrocyte dysfunction, which ultimately lead to neuronal injury and death. In patients effectively treated with antiretroviral therapy, frank dementia is now uncommon and has been replaced by milder forms of neurocognitive impairment, with less frequent and more focal neuropathology. This review summarizes key findings that support the critical role and mechanisms of monocyte/macrophage activation and inflammation as a major component for HIV-1 encephalitis or HIV-1 associated dementia.

Indexed as

AnimalsCentral Nervous System Viral DiseasesHIV-1HIV InfectionsHumansInflammationMacrophagesMicroglia

Identifiers

PMID19768553
PMCPMC5935112
OpenAlexW1988165884

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.