Evidence map›Paper›PMID 18508884›Full record

ArticleJournal of virology2008

Human immunodeficiency virus type 1 infection increases the in vivo capacity of peripheral monocytes to cross the blood-brain barrier into the brain and the in vivo sensitivity of the blood-brain barrier to disruption by lipopolysaccharide.

Hongwei Wang, Jinglin Sun, Harris Goldstein

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

62 citing papers in PubMed, 91 citations in OpenAlex.

  1. Article
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  7. Unraveling the complexities of neurotropic virus infection and immune evasion.Microbiology and molecular biology reviews : MMBR · 2025
    Review
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  19. Treg Cells Attenuate Neuroinflammation and Protect Neurons in a Mouse Model of Parkinson's Disease.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2020
    Article
  20. Article

2 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

3 authors at 1 institution in 1 country.

Hongwei WangDepartment of Microbiology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
Jinglin Sun
Harris Goldstein
Albert Einstein College of Medicine · US

Funding

Immunology/Pathology CoreP30AI051519 · NIAID · YESHIVA UNIVERSITY · PI GOLDSTEIN, HARRIS · 2003 to 2013
$18.6M
Mechanisms of in vivo protection from HIV infectionR01AI067136 · NIAID · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI GOLDSTEIN, HARRIS · 2007 to 2010
$1.6M
TRANSGENIC MICE--MODEL FOR STUDYING HIV INFECTION OF THER01NS039201 · NINDS · YESHIVA UNIVERSITY · PI GOLDSTEIN, HARRIS · 1999 to 2003
$1.3M
NIAID NIH HHS AI067136NIAID NIH HHS AI51519NIAID NIH HHS P30 AI051519NIAID NIH HHS R01 AI067136NINDS NIH HHS NS39201NINDS NIH HHS R01 NS039201
6 · The paper itself

Abstract

Human immunodeficiency virus type 1 (HIV-1), introduced into the brain by HIV-1-infected monocytes which migrate across the blood-brain barrier (BBB), infects resident macrophages and microglia and initiates a process that causes HIV-1-associated neurocognitive disorders. The mechanism by which HIV-1 infection circumvents the BBB-restricted passage of systemic leukocytes into the brain and disrupts the integrity of the BBB is not known. Circulating lipopolysaccharide (LPS), which can compromise the integrity of the BBB, is significantly increased in HIV-1-infected individuals. We hypothesized that HIV-1 infection increases monocyte capacity to migrate across the BBB, which is further facilitated by a compromise of BBB integrity mediated by the increased systemic LPS levels present in HIV-1-infected individuals. To investigate this possibility, we examined the in vivo BBB migration of monocytes derived from our novel mouse model, JR-CSF/EYFP mice, which are transgenic for both a long terminal repeat-regulated full-length infectious HIV-1 provirus and ROSA-26-regulated enhanced yellow fluorescent protein. We demonstrated that JR-CSF/EYFP mouse monocytes displayed an increased capacity to enter the brain by crossing either an intact BBB or a BBB whose integrity was partially compromised by systemic LPS. We also demonstrated that the JR-CSF mouse BBB was more susceptible to disruption by systemic LPS than the control wild-type mouse BBB. These results demonstrated that HIV-1 infection increased the ability of monocytes to enter the brain and increased the sensitivity of the BBB to disruption by systemic LPS, which is elevated in HIV-1-infected individuals. These mice represent a new in vivo system for studying the mechanism by which HIV-1-infected monocytes migrate into the brain.

Indexed as

Disease Models, AnimalAnimalsBlood-Brain BarrierBrainHIV-1HIV InfectionsHumansLipopolysaccharidesMiceMice, TransgenicMonocytesLipopolysaccharides

Identifiers

PMID18508884
PMCPMC2493310
OpenAlexW2097477483

What OpenQuestion holds

Textmetadata
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.