Evidence map›Paper›PMID 24921001›Full record

ReviewWorld journal of biological chemistry2014

Regulation of cell survival and death during Flavivirus infections.

Sounak Ghosh Roy, Beata Sadigh, Emmanuel Datan, Richard A Lockshin, Zahra Zakeri

Open access · diamondAbstract readReview
In one paragraph

Review in World journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
5.5field-weighted citation impact, top 4% 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

32 citing papers in PubMed, 56 citations in OpenAlex.

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  12. Hyperinflammation, apoptosis, and organ damage.Experimental biology and medicine (Maywood, N.J.) · 2022
    Review
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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.

Sounak Ghosh RoySounak Ghosh Roy, Beata Sadigh, Emmanuel Datan, Richard A Lockshin, Zahra Zakeri, Department of Biology, Queens College and Graduate Center of the City University of New York, Queens, New York, NY 11367, United States.
Beata SadighSounak Ghosh Roy, Beata Sadigh, Emmanuel Datan, Richard A Lockshin, Zahra Zakeri, Department of Biology, Queens College and Graduate Center of the City University of New York, Queens, New York, NY 11367, United States.
Emmanuel DatanSounak Ghosh Roy, Beata Sadigh, Emmanuel Datan, Richard A Lockshin, Zahra Zakeri, Department of Biology, Queens College and Graduate Center of the City University of New York, Queens, New York, NY 11367, United States.
Richard A LockshinSounak Ghosh Roy, Beata Sadigh, Emmanuel Datan, Richard A Lockshin, Zahra Zakeri, Department of Biology, Queens College and Graduate Center of the City University of New York, Queens, New York, NY 11367, United States.
Zahra ZakeriSounak Ghosh Roy, Beata Sadigh, Emmanuel Datan, Richard A Lockshin, Zahra Zakeri, Department of Biology, Queens College and Graduate Center of the City University of New York, Queens, New York, NY 11367, United States.
Queens College, CUNY · US

Funding

Characterization of flavovirus NS4A induced autophagyR15AI094351 · NIAID · QUEENS COLLEGE · PI ZAKERI, ZAHRA · 2011 to 2017
$459k
NIAID NIH HHS R15 AI094351
6 · The paper itself

Abstract

Flaviviruses, ss(+) RNA viruses, include many of mankind's most important pathogens. Their pathogenicity derives from their ability to infect many types of cells including neurons, to replicate, and eventually to kill the cells. Flaviviruses can activate tumor necrosis factor α and both intrinsic (Bax-mediated) and extrinsic pathways to apoptosis. Thus they can use many approaches for activating these pathways. Infection can lead to necrosis if viral load is extremely high or to other types of cell death if routes to apoptosis are blocked. Dengue and Japanese Encephalitis Virus can also activate autophagy. In this case the autophagy temporarily spares the infected cell, allowing a longer period of reproduction for the virus, and the autophagy further protects the cell against other stresses such as those caused by reactive oxygen species. Several of the viral proteins have been shown to induce apoptosis or autophagy on their own, independent of the presence of other viral proteins. Given the versatility of these viruses to adapt to and manipulate the metabolism, and thus to control the survival of, the infected cells, we need to understand much better how the specific viral proteins affect the pathways to apoptosis and autophagy. Only in this manner will we be able to minimize the pathology that they cause.

Indexed as

ApoptosisAutophagyDengue virusExtrinsic pathwayFlavivirusIntrinsic pathwayJapanese encephalitis virusNecrosisProgrammed cell deathWest Nile virus

Identifiers

PMID24921001
PMCPMC4050121
OpenAlexW1916166684

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.