Evidence map›Paper›PMID 25798530›Full record

ReviewVirology2015

The role of PI3K/Akt in human herpesvirus infection: From the bench to the bedside.

XueQiao Liu, Jeffrey I Cohen

Open access · greenAbstract 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 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed
4.2field-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

78 citing papers in PubMed, 112 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Akt isoform specificity drives intrinsic immune regulation during HSV-1 infection.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. HerpDock: A GUI-based gateway to HSV-1 molecular docking insights.Computational and structural biotechnology journal · 2024
    Article
  20. Article

18 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

2 authors at 1 institution in 1 country.

XueQiao LiuMedical Virology Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, 20892, USA.
Jeffrey I CohenMedical Virology Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, 20892, USA. Electronic address: jcohen@niaid.nih.gov.
National Institutes of Health · US

Funding

Epstein-Barr Virus Associated DisordersZIAAI000913 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI COHEN, JEFFREY · 2009 to 2025
$14.3M
Herpesvirus Pathogenesis and Vaccine DevelopmentZIAAI000978 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI COHEN, JEFFREY · 2009 to 2025
$13.7M
Pathogenesis and Chemotherapy of Human Virus InfectionsZIAAI000058 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI COHEN, JEFFREY · 2009 to 2025
$8.8M
Molecular Biology Of Varicella Zoster Virus InfectionZIAAI000430 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI COHEN, JEFFREY · 2009 to 2025
$4.5M
THE PATHOGENESIS AND CHEMOTHERAPY OF HERPESVIRUS INFECTIONS IN MANZ01AI000058 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI COHEN, JEFFREY · 1985 to 2008
$680k
Intramural NIH HHS Z01 AI000058
6 · The paper itself

Abstract

The phosphatidylinositol-3-kinase (PI3K)-Akt signaling pathway regulates several key cellular functions including protein synthesis, cell growth, glucose metabolism, and inflammation. Many viruses have evolved mechanisms to manipulate this signaling pathway to ensure successful virus replication. The human herpesviruses undergo both latent and lytic infection, but differ in cell tropism, growth kinetics, and disease manifestations. Herpesviruses express multiple proteins that target the PI3K/Akt cell signaling pathway during the course of their life cycle to facilitate viral infection, replication, latency, and reactivation. Rare human genetic disorders with mutations in either the catalytic or regulatory subunit of PI3K that result in constitutive activation of the protein predispose to severe herpesvirus infections as well as to virus-associated malignancies. Inhibiting the PI3K/Akt pathway or its downstream proteins using drugs already approved for other diseases can block herpesvirus lytic infection and may reduce malignancies associated with latent herpesvirus infections.

Indexed as

Host-Pathogen InteractionsVirus LatencyVirus ReplicationAntiviral AgentsHerpesviridaeHerpesviridae InfectionsHumansOncogene Protein v-aktPhosphatidylinositol 3-KinasePhosphoinositide-3 Kinase InhibitorsSignal TransductionViral ProteinsAntiviral AgentsOncogene Protein v-aktPhosphatidylinositol 3-KinasePhosphoinositide-3 Kinase InhibitorsViral ProteinsAktCytomegalovirusEpstein-Barr virusHerpes simplexHerpesvirusKaposi׳s sarcoma associated herpesvirusPI3KVaricella-zoster

Identifiers

PMID25798530
PMCPMC4424147
OpenAlexW2028483614

What OpenQuestion holds

Textmetadata
LicenceTDM
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.