Evidence map›Paper›PMID 26142496›Full record

ReviewVirology2015

Recent progress in understanding coxsackievirus replication, dissemination, and pathogenesis.

Jon Sin, Vrushali Mangale, Wdee Thienphrapa, Roberta A Gottlieb, Ralph Feuer

Abstract readReview
In one paragraph

Review in Virology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
–field-weighted citation impact
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

67 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Reporter-expressing viruses for antiviral drug discovery research.Frontiers in cellular and infection microbiology · 2025
    Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Antiviral Activity ofAntimicrobial agents and chemotherapy · 2023
    Article
  20. Review

7 more citing papers are in PubMed but not listed here.

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.

Jon SinCedars-Sinai Heart Institute, 8700 Beverly Blvd., Los Angeles, CA 90048, USA.
Vrushali MangaleThe Integrated Regenerative Research Institute (IRRI) at San Diego State University, Cell & Molecular Biology Joint Doctoral Program, Department of Biology, San Diego State University, San Diego, CA 92182-4614, USA.
Wdee ThienphrapaThe Integrated Regenerative Research Institute (IRRI) at San Diego State University, Cell & Molecular Biology Joint Doctoral Program, Department of Biology, San Diego State University, San Diego, CA 92182-4614, USA.
Roberta A GottliebCedars-Sinai Heart Institute, 8700 Beverly Blvd., Los Angeles, CA 90048, USA.
Ralph FeuerThe Integrated Regenerative Research Institute (IRRI) at San Diego State University, Cell & Molecular Biology Joint Doctoral Program, Department of Biology, San Diego State University, San Diego, CA 92182-4614, USA. Electronic address: rfeuer@mail.sdsu.edu.

Funding

Juvenile mouse model of delayed anthracycline cardiotoxicityR01HL092136 · NHLBI · SAN DIEGO STATE UNIVERSITY · PI GOTTLIEB, ROBERTA A., GUSTAFSSON, ASA B. · 2009 to 2013
$1.8M
Coxsackievirus Latency, Immune Activation and Pathogenesis in the CNSR01NS054108 · NINDS · SAN DIEGO STATE UNIVERSITY · PI FEUER, RALPH · 2007 to 2011
$1.5M
NHLBI NIH HHS R01 HL092136NINDS NIH HHS NS054108NINDS NIH HHS R01 NS054108
6 · The paper itself

Abstract

Coxsackieviruses (CVs) are relatively common viruses associated with a number of serious human diseases, including myocarditis and meningo-encephalitis. These viruses are considered cytolytic yet can persist for extended periods of time within certain host tissues requiring evasion from the host immune response and a greatly reduced rate of replication. A member of Picornaviridae family, CVs have been historically considered non-enveloped viruses - although recent evidence suggest that CV and other picornaviruses hijack host membranes and acquire an envelope. Acquisition of an envelope might provide distinct benefits to CV virions, such as resistance to neutralizing antibodies and efficient nonlytic viral spread. CV exhibits a unique tropism for progenitor cells in the host which may help to explain the susceptibility of the young host to infection and the establishment of chronic disease in adults. CVs have also been shown to exploit autophagy to maximize viral replication and assist in unconventional release from target cells. In this article, we review recent progress in clarifying virus replication and dissemination within the host cell, identifying determinants of tropism, and defining strategies utilized by the virus to evade the host immune response. Also, we will highlight unanswered questions and provide future perspectives regarding the potential mechanisms of CV pathogenesis.

Indexed as

Virus InternalizationVirus ReleaseVirus ReplicationAutophagyCoxsackievirus InfectionsEnterovirusHumansImmune EvasionViral TropismAutophagyCardiac progenitor cellsCoxsackievirusEnterovirusMeningoencephalitisMicrovesiclesMyocarditisNeural progenitor cellsPicornavirusVirus dissemination

Identifiers

PMID26142496
PMCPMC4567421

What OpenQuestion holds

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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.