Evidence map›Paper›PMID 31652847›Full record

ArticleViruses2019

In-Vitro Subtype-Specific Modulation of HIV-1 Trans-Activator of Transcription (Tat) on RNAi Silencing Suppressor Activity and Cell Death.

Larance Ronsard, Ashraf S Yousif, Janani Ramesh, N Sumi, Matthew Gorman, Vishnampettai G Ramachandran, Akhil C Banerjea

Open access · goldAbstract read
In one paragraph

Article in Viruses, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.3field-weighted citation impact, top 43% 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

9 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Article
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  4. Protective association of theFrontiers in medicine · 2026
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  5. Exome sequencing-based identification ofFrontiers in molecular biosciences · 2026
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  6. Article
  7. Review
  8. Addressing an HIV cure in LMIC.Retrovirology · 2021
    Review
  9. 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

7 authors at 5 institutions in 2 countries.

Larance RonsardLaboratory of Virology, National Institute of Immunology, New Delhi 110067, India. LRonsard@mgh.harvard.edu.
Ashraf S YousifRagon Institute of MGH, MIT and Harvard University, 400 Technology Square, Cambridge, MA 02139, USA. AHAMADELNEEL@mgh.harvard.edu.
Janani RameshRenal Division, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. rjjananiramesh95@gmail.com.
N SumiEndocrinology & Toxicology Lab, Department of Zoology, University of Calicut, Kerala 673635, India. sumikrishna24@gmail.com.
Matthew GormanRagon Institute of MGH, MIT and Harvard University, 400 Technology Square, Cambridge, MA 02139, USA. mgorman8@mgh.harvard.edu.
Vishnampettai G RamachandranDepartment of Microbiology, University College of Medical Sciences and Guru Teg Bahadur Hospital, Delhi 110095, India. sumikrishna24@gmail.com.
Akhil C BanerjeaLaboratory of Virology, National Institute of Immunology, New Delhi 110067, India. LRonsard@broadinstitute.org.
Ragon Institute of MGH, MIT and Harvard · USUniversity College of Medical Sciences · INBrigham and Women's Hospital · USNational Institute of Immunology · INUniversity of Calicut · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human immunodeficiency virus (HIV) is a global health concern affecting millions of individuals with a wide variety of currently circulating subtypes affecting various regions of the globe. HIV relies on multiple regulatory proteins to modify the host cell to promote replication in infected T cells, and these regulatory proteins can have subtle phenotypic differences between subtypes. One of these proteins, HIV-1 Trans-Activator of Transcription (Tat), is capable of RNA interference (RNAi) Silencing Suppressor (RSS) activity and induction of cell death in T cells. However, the subtype-specific RSS activity and induction of cell death have not been explored. We investigated the ability of Tat subtypes and variants to induce RSS activity and cell death. TatB, from HIV-1 subtype B, was found to be a potent RSS activator by 40% whereas TatC, from HIV-1 subtype C, showed 15% RSS activity while subtype TatC variants exhibited varying levels. A high level of cell death (50-53%) was induced by subtype TatB when compared to subtype TatC (25-28%) and varying levels were observed with subtype TatC variants. These differential activities could be due to variations in the functional domains of Tat. These observations further our understanding of subtype-specific augmentation of Tat in HIV-1 replication and pathogenesis.

Indexed as

RNA InterferenceCell DeathHIV-1HIV InfectionsHost-Parasite InteractionsHumansSpecies Specificitytat Gene Products, Human Immunodeficiency Virustat Gene Products, Human Immunodeficiency Virusacquired immunodeficiency syndrome (AIDS)human immunodeficiency virus (HIV)-1RNA interference (RNAi) silencing suppressor (RSS) activity and cell deathtrans-activator of transcription (Tat) gene

Identifiers

PMID31652847
PMCPMC6893708
OpenAlexW2981686837

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.