Evidence map›Paper›PMID 19004944›Full record

ArticleJournal of virology2009

Human cytomegalovirus-encoded immune modulators partner to downregulate major histocompatibility complex class I molecules.

Vanessa M Noriega, Domenico Tortorella

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.8field-weighted citation impact, top 24% 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

13 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Immune regulation and evasion of Mammalian host cell immunity during viral infection.Indian journal of virology : an official organ of Indian Virological Society · 2013
    Article
  10. Review
  11. Article
  12. Glioma-associated cytomegalovirus mediates subversion of the monocyte lineage to a tumor propagating phenotype.Clinical cancer research : an official journal of the American Association for Cancer Research · 2011
    Article
  13. Modulation of natural killer cell activity by viruses.Current opinion in microbiology · 2010
    Review
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.

Vanessa M NoriegaDepartment of Microbiology, Mount Sinai School of Medicine, New York, New York 10029, USA.
Domenico Tortorella
Icahn School of Medicine at Mount Sinai · US

Funding

Technological Development ComponentU19AI062623 · NIAID · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI MORAN, THOMAS M · 2004 to 2009
$21.3M
Down-regulation of MHC class l molecules by HCMV US2R01AI060905 · NIAID · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI TORTORELLA, DOMENICO · 2005 to 2009
$1.8M
NIAID NIH HHS AI060905NIAID NIH HHS AI060905-SINIAID NIH HHS R01 AI060905NIAID NIH HHS U19 AI062623NIAID NIH HHS U19 AI62623
6 · The paper itself

Abstract

Throughout the course of natural evolution with its host, the human cytomegalovirus (HCMV) has developed a variety of strategies to avoid immune recognition and clearance. The major histocompatibility complex (MHC) class I antigen presentation pathway is a major target of the virus. HCMV encodes at least six gene products that modulate the processing of endoplasmic reticulum (ER)-resident MHC class I molecules. Here, we show that two virus-encoded proteins, US2 and US3, coordinate their functions toward the common goal of attenuating class I protein surface expression. In cells stably expressing both US2 and US3, class I molecules were almost completely downregulated from the cell surface. In addition, pulse-chase analysis revealed that the proteasome-dependent turnover of class I molecules occurs more rapidly in cells expressing both US2 and US3 than either US2 or US3 alone. The ability of US3 to retain class I molecules in the ER produces a target-rich environment for US2 to mediate the destruction of class I heavy chains. In fact, expression of US3 enhanced the association between US2 and class I molecules, thus encouraging their dislocation and degradation. This immune evasion strategy ensures that viral antigens are not presented on the cell surface during the early phase of HCMV infection, a critical time of replication and viral proliferation.

Indexed as

Down-RegulationAstrocytomaCell Line, TumorCytomegalovirusFlow CytometryGlycoproteinsHistocompatibility Antigens Class IHumansHydrolysisImmediate-Early ProteinsImmunoprecipitationMembrane ProteinsViral Envelope ProteinsGlycoproteinsHistocompatibility Antigens Class IImmediate-Early ProteinsMembrane ProteinsUS2 protein, VaricellovirusUS3 protein, cytomegalovirusViral Envelope Proteins

Identifiers

PMID19004944
PMCPMC2620908
OpenAlexW2171532735

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.