Evidence map›Paper›PMID 26848681›Full record

ArticleViruses2016

Pandemic Influenza A (H1N1) Virus Infection Increases Apoptosis and HIV-1 Replication in HIV-1 Infected Jurkat Cells.

Xue Wang, Jiying Tan, Santanu Biswas, Jiangqin Zhao, Krishnakumar Devadas, Zhiping Ye, Indira Hewlett

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Viruses, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

6 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. [Advances in application of Jurkat cell model in research on infectious diseases].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2018
    Review
  6. 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 1 institution in 1 country.

Xue WangLab of Molecular Virology, Division of Emerging and Transfusion Transmitted Diseases, CBER/FDA, Building 72, Rm 4322, 10903 New Hampshire Avenue, Silver Spring, MD 20993, USA. xue.wang@fda.hhs.gov.
Jiying TanLab of Molecular Virology, Division of Emerging and Transfusion Transmitted Diseases, CBER/FDA, Building 72, Rm 4322, 10903 New Hampshire Avenue, Silver Spring, MD 20993, USA. tangjy@lzu.edu.cn.
Santanu BiswasLab of Molecular Virology, Division of Emerging and Transfusion Transmitted Diseases, CBER/FDA, Building 72, Rm 4322, 10903 New Hampshire Avenue, Silver Spring, MD 20993, USA. Santanu.biswas@fda.hhs.gov.
Jiangqin ZhaoLab of Molecular Virology, Division of Emerging and Transfusion Transmitted Diseases, CBER/FDA, Building 72, Rm 4322, 10903 New Hampshire Avenue, Silver Spring, MD 20993, USA. Jiangqin.zhao@fda.hhs.gov.
Krishnakumar DevadasLab of Molecular Virology, Division of Emerging and Transfusion Transmitted Diseases, CBER/FDA, Building 72, Rm 4322, 10903 New Hampshire Avenue, Silver Spring, MD 20993, USA. Krishnakumar.devada@fda.hhs.gov.
Zhiping YeDivision of Viral Products, Center for Biologics Evaluation and Research, Food and Drug Administration, Silver Spring, MD 20993, USA. zhiping.ye@fda.hhs.gov.
Indira HewlettLab of Molecular Virology, Division of Emerging and Transfusion Transmitted Diseases, CBER/FDA, Building 72, Rm 4322, 10903 New Hampshire Avenue, Silver Spring, MD 20993, USA. indira.hewlett@fda.hhs.gov.
Center for Biologics Evaluation and Research · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Influenza virus infection has a significant impact on public health, since it is a major cause of morbidity and mortality. It is not well-known whether influenza virus infection affects cell death and human immunodeficiency virus (HIV)-1 replication in HIV-1-infected patients. Using a lymphoma cell line, Jurkat, we examined the in vitro effects of pandemic influenza A (H1N1) virus (pH1N1) infection on cell death and HIV-1 RNA production in infected cells. We found that pH1N1 infection increased apoptotic cell death through Fas and Bax-mediated pathways in HIV-1-infected Jurkat cells. Infection with pH1N1 virus could promote HIV-1 RNA production by activating host transcription factors including nuclear factor kappa-light-chain-enhancer of activated B cells (NF-ĸB), nuclear factor of activated T-cells (NFAT) and activator protein 1 (AP-1) through mitogen-activated protein kinases (MAPK) pathways and T-cell antigen receptor (TCR)-related pathways. The replication of HIV-1 latent infection could be reactivated by pH1N1 infection through TCR and apoptotic pathways. These data indicate that HIV-1 replication can be activated by pH1N1 virus in HIV-1-infected cells resulting in induction of cell death through apoptotic pathways.

Indexed as

ApoptosisAnimalsCell LineChick EmbryoCoinfectionGlobal HealthHIV-1HIV InfectionsHumansInfluenza A Virus, H1N1 SubtypeInfluenza, HumanJurkat CellsNFATC Transcription FactorsNF-kappa BNFATC Transcription FactorsNF-kappa BapoptosisCD4HIV-1pandemic influenza A (H1N1) virusreplication

Identifiers

PMID26848681
PMCPMC4776188
OpenAlexW2271237851

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.