Evidence map›Paper›PMID 23152529›Full record

ArticleJournal of virology2013

Herpes simplex virus 2 (HSV-2) prevents dendritic cell maturation, induces apoptosis, and triggers release of proinflammatory cytokines: potential links to HSV-HIV synergy.

Martha Stefanidou, Irene Ramos, Veronica Mas Casullo, Janie B Trépanier, Sara Rosenbaum, Ana Fernandez-Sesma, Betsy C Herold

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
4.9field-weighted citation impact, top 5% 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

48 citing papers in PubMed, 67 citations in OpenAlex.

  1. Trial
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  6. Review
  7. Antiviral activity of red algae phycocolloids against herpes simplex virus type 2Biotechnology reports (Amsterdam, Netherlands) · 2023
    Article
  8. Article
  9. CD83 Regulates the Immune Responses in Inflammatory Disorders.International journal of molecular sciences · 2023
    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

7 authors at 2 institutions in 1 country.

Martha StefanidouDepartments of Pediatrics and Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, New York, USA. martha.stefanidou@einstein.yu.edu
Irene Ramos
Veronica Mas Casullo
Janie B Trépanier
Sara Rosenbaum
Ana Fernandez-Sesma
Betsy C Herold
Albert Einstein College of Medicine · USIcahn School of Medicine at Mount Sinai · US

Funding

Impact of HSV-2 on Female Genital Tract Mucosal Immunity & HIV InfectionR01AI065309 · NIAID · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI HEROLD, BETSY C. · 2005 to 2014
$5.1M
Molecular & Developmental Biology in Pediatric ResearchK12HD052890 · NICHD · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI SATLIN, LISA M. · 2006 to 2010
$2.1M
Role of Calcium Signaling in HSV-2 InvasionR01AI061679 · NIAID · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI HEROLD, BETSY C. · 2005 to 2009
$1.8M
Role of Calcium Signaling in HSV-2 InvasionR56AI061679 · NIAID · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI HEROLD, BETSY C. · 2010 to 2010
$408k
NIAID NIH HHS AI061679NIAID NIH HHS AI65309NIAID NIH HHS HHSN266200700010CNIAID NIH HHS R01 AI061679NIAID NIH HHS R01 AI065309NIAID NIH HHS R56 AI061679NICHD NIH HHS K12 HD052890
6 · The paper itself

Abstract

Herpes simplex virus 2 (HSV-2) may cause frequent recurrences, highlighting its ability to evade host defense. This study tested the hypothesis that HSV-2 interferes with dendritic cell (DC) function as an escape mechanism, which may contribute to enhanced HIV replication in coinfected populations. Immature monocyte-derived human DCs were exposed to live or UV-inactivated HSV-2 or lipopolysaccharide. Little or no increase in the maturation marker CD83 was observed in response to HSV-2 and HSV-2 exposed DCs were impaired in their ability to present antigen (influenza) to T cells. Exposure to UV-inactivated virus stimulated a modest, but significant increase in CD83, suggesting that viral gene expression contributes to the block in DC maturation. The functional impairment of HSV-2-exposed DCs could be partially attributed to the induction of apoptosis. Live and inactivated HSV-2 triggered an increase in the number of early and late apoptotic cells in both the infected and bystander cell populations; apoptosis was associated with a decrease in cellular FLICE-inhibitory protein (c-FLIP). Paradoxically, HSV-2 induced Akt phosphorylation, which typically promotes DC maturation and survival. Despite these aberrant responses, live and inactivated HSV-2 induced the release of cytokines into culture supernatants, which were sufficient to activate HIV-1 replication in latently infected U1 cells. Together, these findings suggest that in the presence of overt or subclinical HSV-2, the function of mucosal DCs would be impaired. These responses may allow HSV to escape immune surveillance but may also promote HIV infection and contribute to the epidemiological link between HIV and HSV.

Indexed as

ApoptosisImmune EvasionAntigen PresentationAntigens, CDCD83 AntigenCells, CulturedCytokinesDendritic CellsHerpesvirus 2, HumanHIV-1HumansImmunoglobulinsMembrane GlycoproteinsVirus ReplicationAntigens, CDCD83 AntigenCytokinesImmunoglobulinsMembrane Glycoproteins

Identifiers

PMID23152529
PMCPMC3554174
OpenAlexW2050332051

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.