Evidence map›Paper›PMID 17080326›Full record

ArticleApoptosis : an international journal on programmed cell death2007

Herpes simplex virus blocks apoptosis by precluding mitochondrial cytochrome c release independent of caspase activation in infected human epithelial cells.

Martine Aubert, Lisa E Pomeranz, John A Blaho

Abstract read
In one paragraph

Article in Apoptosis : an international journal on programmed cell death, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing 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

22 citing papers in PubMed.

  1. Cell death network regulation in HSV infection: immune evasion versus host defense.Apoptosis : an international journal on programmed cell death · 2026
    Review
  2. Review
  3. Review
  4. Clinical Management of Herpes Simplex Virus Keratitis.Diagnostics (Basel, Switzerland) · 2022
    Review
  5. The Possible Role of Neural Cell Apoptosis in Multiple Sclerosis.International journal of molecular sciences · 2022
    Review
  6. Observational
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
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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

3 authors.

Martine AubertDepartment of Microbiology, Mount Sinai School of Medicine, One Gustave L. Levy Place, Box 1124, New York, NY 10029-6574, USA.
Lisa E Pomeranz
John A Blaho

Funding

TRAINING PROGRAM IN CELLULAR AND MOLECULAR BIOLOGYT32GM008553 · NIGMS · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI MLODZIK, MAREK · 1995 to 2012
$1.6M
HSV REGULATION BY PROTEIN MODIFICATIONR01AI038873 · NIAID · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI BLAHO, JOHN A. · 2002 to 2006
$1.5M
APOPTOSIS DURING HSV INFECTIONR01AI048582 · NIAID · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI BLAHO, JOHN A. · 2002 to 2006
$1.5M
HSV REGULATION BY PROTEIN MODIFICATIONR21AI038873 · NIAID · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI BLAHO, JOHN A. · 2001 to 2001
$339k
HSV PROTEIN NUCLEOTIDYLATION AND LYTIC INFECTIONR29AI038873 · NIAID · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI BLAHO, JOHN A. · 1996 to 2000
$117k
NIAID NIH HHS AI38873NIAID NIH HHS AI48582NIAID NIH HHS R01 AI038873NIAID NIH HHS R01 AI048582NIAID NIH HHS R21 AI038873NIAID NIH HHS R29 AI038873NIGMS NIH HHS GM08553NIGMS NIH HHS T32 GM008553
6 · The paper itself

Abstract

Expression of HSV-1 genes leads to the induction of apoptosis in human epithelial HEp-2 cells but the subsequent synthesis of infected cell protein prevents the process from killing the cells. Thus, viruses unable to produce appropriate prevention factors are apoptotic. We now report that the addition of either a pancaspase inhibitor or caspase-9-specific inhibitor prevented cells infected with an apoptotic HSV-1 virus from undergoing cell death. This result indicated that HSV-1-dependent apoptosis proceeds through the mitochondrial apoptotic pathway. However, the pancaspase inhibitor did not prevent the release of cytochrome c from mitochondria, implying that caspase activation is not required for this induction of cytochrome c release by HSV-1. The release of cytochrome c was first detected at 9 hpi while caspase-9, caspase-3 and PARP processing were detected at 12 hpi. Finally, Bax accumulated at mitochondria during apoptotic, but not wild type HSV-1 infection. Together, these findings indicate that HSV-1 blocks apoptosis by precluding mitochondrial cytochrome c release in a caspase-independent manner and suggest Bax as a target in infected human epithelial cells.

Indexed as

Apoptosisbcl-2-Associated X ProteinCaspase 9Caspase InhibitorsCaspasesCell LineCytochromes cDefective VirusesEnzyme ActivationEpithelial CellsHerpes SimplexHerpesvirus 1, HumanHumansMitochondriaBAX protein, humanbcl-2-Associated X ProteinCaspase 9Caspase InhibitorsCaspasesCytochromes c

Identifiers

PMID17080326
PMCPMC2799008

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.