Evidence map›Paper›PMID 22787205›Full record

ArticleJournal of virology2012

HIV-1 induces telomerase activity in monocyte-derived macrophages, possibly safeguarding one of its reservoirs.

Rita Reynoso, Matthias Wieser, Diego Ojeda, Maximilian Bönisch, Harald Kühnel, Federico Bolcic, Heribert Quendler, Johannes Grillari, Regina Grillari-Voglauer, Jorge Quarleri

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

30 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. HIV-Infected Patients as a Model of Aging.Microbiology spectrum · 2023
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Current and Future Therapeutic Strategies for Lentiviral Eradication from Macrophage Reservoirs.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2019
    Review
  17. Article
  18. Article
  19. Review
  20. Article
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

10 authors at 5 institutions in 2 countries.

Rita ReynosoAging and Immortalization Research, Department of Biotechnology, University of Natural Resources and Life Sciences Vienna, Vienna, Austria.
Matthias Wieser
Diego Ojeda
Maximilian Bönisch
Harald Kühnel
Federico Bolcic
Heribert Quendler
Johannes Grillari
Regina Grillari-Voglauer
Jorge Quarleri
BOKU University · ATConsejo Nacional de Investigaciones Científicas y Técnicas · ARUniversity of Buenos Aires · AREvercyte (Austria) · ATUniversity of Veterinary Medicine Vienna · AT

Funding

Austrian Science Fund FWF I 510
6 · The paper itself

Abstract

Monocyte-derived macrophages (MDM) are widely distributed in all tissues and organs, including the central nervous system, where they represent the main part of HIV-infected cells. In contrast to activated CD4(+) T lymphocytes, MDM are resistant to cytopathic effects and survive HIV infection for a long period of time. The molecular mechanisms of how HIV is able to persist in macrophages are not fully elucidated yet. In this context, we have studied the effect of in vitro HIV-1 infection on telomerase activity (TA), telomere length, and DNA damage. Infection resulted in a significant induction of TA. This increase was directly proportional to the efficacy of HIV infection and was found in both nuclear and cytoplasmic extracts, while neither UV light-inactivated HIV nor exogenous addition of the viral protein Tat or gp120 affected TA. Furthermore, TA was not modified during monocyte-macrophage differentiation, MDM activation, or infection with vaccinia virus. HIV infection did not affect telomere length. However, HIV-infected MDM showed less DNA damage after oxidative stress than noninfected MDM, and this resistance was also increased by overexpressing telomerase alone. Taken together, our results suggest that HIV induces TA in MDM and that this induction might contribute to cellular protection against oxidative stress, which could be considered a viral strategy to make macrophages better suited as longer-lived, more resistant viral reservoirs. In the light of the clinical development of telomerase inhibitors as anticancer therapeutics, inhibition of TA in HIV-infected macrophages might also represent a novel therapeutic target against viral reservoirs.

Indexed as

Gene Expression Regulation, ViralCD4-Positive T-LymphocytesCell NucleusCytoplasmDNA DamageHIV-1HIV InfectionsHumansInterleukin-4LipopolysaccharidesMacrophagesOxidative StressPhenotypeTelomeraseTelomereInterleukin-4LipopolysaccharidesTelomerase

Identifiers

PMID22787205
PMCPMC3457250
OpenAlexW2122511422

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.