Evidence map›Paper›PMID 22497807›Full record

ArticleMolecular immunology2012

Human cytomegalovirus US3 modulates destruction of MHC class I molecules.

Vanessa M Noriega, Julia Hesse, Thomas J Gardner, Katrin Besold, Bodo Plachter, Domenico Tortorella

Abstract read
In one paragraph

Article in Molecular immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

32 citing papers in PubMed, 38 citations in OpenAlex.

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  11. Evasion of the Host Immune Response by Betaherpesviruses.International journal of molecular sciences · 2021
    Review
  12. Battle between Host Immune Cellular Responses and HCMV Immune Evasion.International journal of molecular sciences · 2019
    Review
  13. Article
  14. Article
  15. Immune Ecosystem of Virus-Infected Host Tissues.International journal of molecular sciences · 2018
    Review
  16. Review
  17. Article
  18. 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

6 authors at 3 institutions in 2 countries.

Vanessa M NoriegaMount Sinai School of Medicine, Department of Microbiology, New York, NY 10029, USA.
Julia Hesse
Thomas J Gardner
Katrin Besold
Bodo Plachter
Domenico Tortorella
Icahn School of Medicine at Mount Sinai · USJohannes Gutenberg University Mainz · DEUniversity Medical Center of the Johannes Gutenberg University Mainz · DE

Funding

TRAINING PROGRAM: MECHANISMS OF VIRUS-HOST INTERACTIONST32AI007647 · NIAID · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI Domenico Tortorella · 2000 to 2026
$11.5M
Translational Immunology Training ProgramT32AI078892 · NIAID · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI Karen Leigh Edelblum, SERGIO A. LIRA · 2008 to 2026
$4.5M
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
Identification of Inhibitors that Stabilize ER Degradation SubstratesR03MH094186 · NIMH · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI TORTORELLA, DOMENICO · 2011 to 2012
$85k
NIAID NIH HHS AI060905NIAID NIH HHS R01 AI060905NIAID NIH HHS T32 AI007647NIAID NIH HHS T32-AI07647NIAID NIH HHS T32 AI078892NIAID NIH HHS T32-AI078892NIMH NIH HHS R03 MH094186
6 · The paper itself

Abstract

Human cytomegalovirus (HCMV), a member of the Herpesviridae family, is proficient at establishing lifelong persistence within the host in part due to immune modulating genes that limit immune recognition. HCMV encodes at least five glycoproteins within its unique short (US) genomic region that interfere with MHC class I antigen presentation, thus hindering viral clearance by cytotoxic T lymphocytes (CTL). Specifically, US3 retains class I within the endoplasmic reticulum (ER), while US2 and US11 induce class I heavy chain destruction. A cooperative effect on class I down-regulation during stable expression of HCMV US2 and US3 has been established. To address the impact of US3 on US11-mediated MHC class I down-regulation, the fate of class I molecules was examined in US3/US11-expressing cells and virus infection studies. Co-expression of US3 and US11 resulted in a decrease of surface expression of class I molecules. However, the class I molecules in US3/US11 cells were mostly retained in the ER with an attenuated rate of proteasome destruction. Analysis of class I levels from virus-infected cells using HCMV variants either expressing US3 or US11 revealed efficient surface class I down-regulation upon expression of both viral proteins. Cells infected with both US3 and US11 expressing viruses demonstrate enhanced retention of MHC class I complexes within the ER. Collectively, the data suggests a paradigm where HCMV-induced surface class I down-regulation occurs by diverse mechanisms dependent on the expression of specific US genes. These results validate the commitment of HCMV to limiting the surface expression of class I levels during infection.

Indexed as

Cell LineCytomegalovirusFluorescent Antibody TechniqueGenes, ViralHistocompatibility Antigens Class IHumansViral ProteinsHistocompatibility Antigens Class IViral Proteins

Identifiers

PMID22497807
PMCPMC3367378
OpenAlexW1992620035

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.