Evidence map›Paper›PMID 32098055›Full record

ArticleViruses2020

Extracellular Vesicles from Human Papilloma Virus-Infected Cervical Cancer Cells Enhance HIV-1 Replication in Differentiated U1 Cell Line.

Sabina Ranjit, Sunitha Kodidela, Namita Sinha, Subhash Chauhan, Santosh Kumar

Open access · goldAbstract read
In one paragraph

Article in Viruses, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

18 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. Impact of HIV on HPV-related cancers in men who have sex with men: a review.Frontiers in cellular and infection microbiology · 2024
    Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. HPV-Related Cervical Cancer and Extracellular Vesicles.Diagnostics (Basel, Switzerland) · 2022
    Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. Extracellular Vesicles in Viral Infections: Two Sides of the Same Coin?Frontiers in cellular and infection microbiology · 2020
    Review
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

5 authors at 1 institution in 1 country.

Sabina RanjitDepartment of Pharmaceutical Sciences, University of Tennessee Health Science Center, Memphis, TN 38163, USA.
Sunitha KodidelaDepartment of Pharmaceutical Sciences, University of Tennessee Health Science Center, Memphis, TN 38163, USA.ORCID 0000-0002-9385-5985
Namita SinhaDepartment of Pharmaceutical Sciences, University of Tennessee Health Science Center, Memphis, TN 38163, USA.
Subhash ChauhanDepartment of Pharmaceutical Sciences, University of Tennessee Health Science Center, Memphis, TN 38163, USA.
Santosh KumarDepartment of Pharmaceutical Sciences, University of Tennessee Health Science Center, Memphis, TN 38163, USA.
University of Tennessee Health Science Center · US

Funding

Monocytic and exosomal cytochrome P450s in smoking-mediated HIV-1 pathogenesisR01DA047178 · NIDA · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI CORY, THEODORE, KUMAR, SANTOSH · 2018 to 2022
$1.7M
6 · The paper itself

Abstract

In the current study, we hypothesized that extracellular vesicles (EVs) secreted from human papilloma virus (HPV)-infected cervical cancer cells exacerbate human immunodeficiency virus (HIV)-1 replication in differentiated U1 cell line through an oxidative stress pathway. To test the hypothesis, we treated an HIV-1-infected macrophage cell line (U1) with HPV-infected Caski cell culture supernatant (CCS). We observed a significant increase in HIV-1 replication, which was associated with an increase in the expression of cytochrome P450 (CYPs 1A1 and 2A6) in the CCS-treated U1 cells. Furthermore, we isolated EVs from CCS (CCS-EVs), which showed the presence of CYPs (1A1, 2A6), superoxide dismutase 1 (SOD1), and HPV oncoproteins HPV16 E6. CCS-EVs when exposed to the U1 cells also significantly increased HIV-1 replication. Treatment of antioxidant, CYP1A1 and CYP2A6 inhibitors, and chemodietary agents with antioxidant properties significantly reduced the CCS and CCS-EVs mediated HIV-1 replication in U1 cells. Altogether, we demonstrate that cervical cancer cells exacerbate HIV-1 replication in differentiated U1 cell line via transferring CYPs and HPV oncoproteins through EVs. We also show that the viral replication occurs via CYP and oxidative stress pathways, and the viral replication is also reduced by chemodietary agents. This study provides important information regarding biological interactions between HPV and HIV-1 via EVs leading to enhanced HIV-1 replication.

Indexed as

Cell DifferentiationOxidative StressVirus ReplicationCervix UteriCulture MediaCytochrome P-450 Enzyme SystemExtracellular VesiclesFemaleHIV-1Human papillomavirus 16HumansMacrophagesOncogene ProteinsPapillomavirus InfectionsU937 CellsUterine Cervical NeoplasmsCulture MediaCytochrome P-450 Enzyme SystemOncogene Proteinscervical cancerCYPsextracellular vesiclesHIVHPVoxidative stress

Identifiers

PMID32098055
PMCPMC7077309
OpenAlexW3007470249

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.