Evidence map›Paper›PMID 20631136›Full record

ArticleJournal of virology2010

Myosin Va enhances secretion of herpes simplex virus 1 virions and cell surface expression of viral glycoproteins.

Kari L Roberts, Joel D Baines

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

40 citing papers in PubMed, 67 citations in OpenAlex.

  1. Article
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  7. Review
  8. Article
  9. Article
  10. Review
  11. HSV-1 Cytoplasmic Envelopment and Egress.International journal of molecular sciences · 2020
    Review
  12. Article
  13. Review
  14. Article
  15. Kinetics of Mimivirus Infection Stages Quantified Using Image Flow Cytometry.Cytometry. Part A : the journal of the International Society for Analytical Cytology · 2019
    Article
  16. Review
  17. Article
  18. Article
  19. 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

2 authors at 1 institution in 1 country.

Kari L RobertsC5132 Vet Med Center, New York State College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA.
Joel D Baines
Cornell University · US

Funding

Nucleocapsid Envelopment Herpes Simplex Virus-1R01AI052341 · NIAID · LOUISIANA STATE UNIV A&M COL BATON ROUGE · PI BAINES, JOEL D. · 2003 to 2013
$3.6M
TRAINING IN MOLECULAR VIROLOGY AND PATHOGENESIST32AI007618 · NIAID · CORNELL UNIVERSITY ITHACA · PI PARRISH, COLIN R. · 2000 to 2010
$1.4M
NIAID NIH HHS R01 AI052341NIAID NIH HHS R01 AI52341NIAID NIH HHS T32 AI007618
6 · The paper itself

Abstract

The final step in the egress of herpes simplex virus (HSV) virions requires virion-laden vesicles to bypass cortical actin and fuse with the plasma membrane, releasing virions into the extracellular space. Little is known about the host or viral proteins involved. In the current study, we noted that the conformation of myosin Va (myoVa), a protein known to be involved in melanosome and secretory granule trafficking to the plasma membrane in melanocytes and neuroendocrine cells, respectively, was altered by 4 h after infection with HSV-1 such that an N-terminal epitope expected to be masked in its inactive state was rendered immunoreactive. Wild-type myoVa localized throughout the cytoplasm and to a limited extent in the nuclei of HSV-infected cells. Two different dominant negative myoVa molecules containing cargo-binding domains but lacking the lever arms and actin-binding domains colocalized with markers of the trans-Golgi network (TGN). Expression of dominant negative myoVa isoforms reduced secretion of HSV-1 infectivity into the medium by 50 to 75%, reduced surface expression of glycoproteins B, M, and D, and increased intracellular virus infectivity to levels consistent with increased retention of virions in the cytoplasm. These data suggest that myoVa is activated during HSV-1 infection to help transport virion- and glycoprotein-laden vesicles from the TGN, through the cortical actin, to the plasma membrane. We cannot exclude a role for myoVa in promoting fusion of these vesicles with the inner surface of the plasma membrane. These data also indicate that myoVa is involved in exocytosis in human epithelial cells as well as other cell types.

Indexed as

Base SequenceBiological Transport, ActiveCell MembraneCytoplasmDNA PrimersEpitopesHeLa CellsHerpesvirus 1, HumanHost-Pathogen InteractionsHumansMembrane FusionMutant ProteinsMyosin Heavy ChainsMyosin Type VRecombinant Proteinstrans-Golgi NetworkDNA PrimersEpitopesMutant ProteinsMYO5A protein, humanMyosin Heavy ChainsMyosin Type VRecombinant ProteinsViral Structural Proteins

Identifiers

PMID20631136
PMCPMC2937760
OpenAlexW2159970977

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.