Evidence map›Paper›PMID 28060843›Full record

ArticlePloS one2017

Modeling the Mechanisms by Which HIV-Associated Immunosuppression Influences HPV Persistence at the Oral Mucosa.

Meghna Verma, Samantha Erwin, Vida Abedi, Raquel Hontecillas, Stefan Hoops, Andrew Leber, Josep Bassaganya-Riera, Stanca M Ciupe

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

17 citing papers in PubMed, 41 citations in OpenAlex.

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  11. Mathematical Modelling of HIV-HCV Coinfection Dynamics in Absence of Therapy.Computational and mathematical methods in medicine · 2020
    Article
  12. Article
  13. Article
  14. Article
  15. Validated Models of Immune Response to Virus Infection.Current opinion in systems biology · 2018
    Article
  16. Modulators of Redox Metabolism in Head and Neck Cancer.Antioxidants & redox signaling · 2018
    Review
  17. 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

8 authors at 2 institutions in 1 country.

Meghna VermaNutritional Immunology and Molecular Medicine Laboratory, Biocomplexity Institute of Virginia Tech, Blacksburg, VA, United States of America.
Samantha ErwinDepartment of Mathematics, Virginia Tech, Blacksburg, VA, United States of America.
Vida AbediNutritional Immunology and Molecular Medicine Laboratory, Biocomplexity Institute of Virginia Tech, Blacksburg, VA, United States of America.
Raquel HontecillasNutritional Immunology and Molecular Medicine Laboratory, Biocomplexity Institute of Virginia Tech, Blacksburg, VA, United States of America.
Stefan HoopsNutritional Immunology and Molecular Medicine Laboratory, Biocomplexity Institute of Virginia Tech, Blacksburg, VA, United States of America.
Andrew LeberNutritional Immunology and Molecular Medicine Laboratory, Biocomplexity Institute of Virginia Tech, Blacksburg, VA, United States of America.
Josep Bassaganya-RieraNutritional Immunology and Molecular Medicine Laboratory, Biocomplexity Institute of Virginia Tech, Blacksburg, VA, United States of America.
Stanca M CiupeDepartment of Mathematics, Virginia Tech, Blacksburg, VA, United States of America.
Virginia Tech · USBiocom · US

Funding

COPASI software for modeling and simulation of biochemical networksR01GM080219 · NIGMS · VIRGINIA POLYTECHNIC INST AND ST UNIV · PI HOOPS, STEFAN, MENDES, PEDRO · 2007 to 2019
$5.4M
NIGMS NIH HHS R01 GM080219
6 · The paper itself

Abstract

Human immunodeficiency virus (HIV)-infected patients are at an increased risk of co-infection with human papilloma virus (HPV), and subsequent malignancies such as oral cancer. To determine the role of HIV-associated immune suppression on HPV persistence and pathogenesis, and to investigate the mechanisms underlying the modulation of HPV infection and oral cancer by HIV, we developed a mathematical model of HIV/HPV co-infection. Our model captures known immunological and molecular features such as impaired HPV-specific effector T helper 1 (Th1) cell responses, and enhanced HPV infection due to HIV. We used the model to determine HPV prognosis in the presence of HIV infection, and identified conditions under which HIV infection alters HPV persistence in the oral mucosa system. The model predicts that conditions leading to HPV persistence during HIV/HPV co-infection are the permissive immune environment created by HIV and molecular interactions between the two viruses. The model also determines when HPV infection continues to persist in the short run in a co-infected patient undergoing antiretroviral therapy. Lastly, the model predicts that, under efficacious antiretroviral treatment, HPV infections will decrease in the long run due to the restoration of CD4+ T cell numbers and protective immune responses.

Indexed as

Anti-HIV AgentsCD4-Positive T-LymphocytesCoinfectionHIV InfectionsHumansImmunocompromised HostModels, BiologicalMouth MucosaOncogenesPapillomaviridaePapillomavirus InfectionsPrognosistat Gene Products, Human Immunodeficiency VirusAnti-HIV Agentstat Gene Products, Human Immunodeficiency Virus

Identifiers

PMID28060843
PMCPMC5218576
OpenAlexW2569973341

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.