Evidence map›Paper›PMID 24639397›Full record

ReviewJournal of neurovirology2014

Complement and HIV-I infection/HIV-associated neurocognitive disorders.

Fengming Liu, Shen Dai, Jennifer Gordon, Xuebin Qin

Open access · greenAbstract readReview
In one paragraph

Review in Journal of neurovirology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 23% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

  1. Pooled it
  2. Review
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  14. The role of the complement system in HIV infection and preeclampsia.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2019
    Review
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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

4 authors at 2 institutions in 2 countries.

Fengming LiuDepartment of Neuroscience, Temple University School of Medicine, Room# 749, 3500 N Broad Street, Philadelphia, PA, 19140, USA.
Shen Dai
Jennifer Gordon
Xuebin Qin
Temple University · USShandong University · CN

Funding

Viral Gene Editing and Bioinformatics Core for Institution # 269291P30MH092177 · NIMH · TEMPLE UNIV OF THE COMMONWEALTH · PI Ilker Kudret Sariyer · 2011 to 2026
$24.9M
Development of Therapeutic CD59 inhibitor for treating B-cell malignanciesR01CA166144 · NCI · TEMPLE UNIV OF THE COMMONWEALTH · PI QIN, XUEBIN · 2013 to 2017
$1.7M
Abrogating human CD59 activity for antibody-based cancer therapyR21CA141324 · NCI · HARVARD MEDICAL SCHOOL · PI QIN, XUEBIN · 2010 to 2011
$399k
NCI NIH HHS 1R01CA166144NCI NIH HHS R01 CA166144NCI NIH HHS R21 CA141324NCI NIH HHS R21CA141324NIMH NIH HHS P30 MH092177
6 · The paper itself

Abstract

The various neurological complications associated with HIV-1 infection, specifically HIV-associated neurocognitive disorders (HAND) persist as a major public health burden worldwide. Despite the widespread use of anti-retroviral therapy, the prevalence of HAND is significantly high. HAND results from the direct effects of an HIV-1 infection as well as secondary effects of HIV-1-induced immune reaction and inflammatory response. Complement, a critical mediator of innate and acquired immunity, plays important roles in defeating many viral infections by the formation of a lytic pore or indirectly by opsonization and recruitment of phagocytes. While the role of complement in the pathogenesis of HIV-1 infection and HAND has been previously recognized for over 15 years, it has been largely underestimated thus far. Complement can be activated through HIV-1 envelope proteins, mannose-binding lectins (MBL), and anti-HIV-1 antibodies. Complement not only fights against HIV-1 infection but also enhances HIV-1 infection. In addition, HIV-1 can hijack complement regulators such as CD59 and CD55 and can utilize these regulators and factor H to escape from complement attack. Normally, complement levels in brain are much lower than plasma levels and there is no or little complement deposition in brain cells. Interestingly, local production and deposition of complement are dramatically increased in HIV-1-infected brain, indicating that complement may contribute to the pathogenesis of HAND. Here, we review the current understanding of the role of complement in HIV-1 infection and HAND, as well as potential therapeutic approaches targeting the complement system for the treatment and eradications of HIV-1 infection.

Indexed as

Adaptive ImmunityAIDS Dementia ComplexAntibodies, ViralAntigen-Antibody ComplexAntigens, CDComplement System ProteinsHIV-1HIV AntibodiesHumansImmune EvasionImmunity, InnateMannose-Binding LectinsViral Envelope ProteinsAntibodies, ViralAntigen-Antibody ComplexAntigens, CDComplement System ProteinsHIV AntibodiesMannose-Binding LectinsViral Envelope Proteins

Identifiers

PMID24639397
PMCPMC4251668
OpenAlexW2051797995

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.