Evidence map›Paper›PMID 35513305›Full record

ReviewClinical immunology (Orlando, Fla.)2022

SARS-CoV-2/COVID-19 and its relationship with NOD2 and ubiquitination.

Edgardo Guzman Rivera, Asha Patnaik, Joann Salvemini, Sanjeev Jain, Katherine Lee, Daniel Lozeau, Qingping Yao

Open access · greenAbstract readReview
In one paragraph

Review in Clinical immunology (Orlando, Fla.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
6.1field-weighted citation impact, top 3% 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

17 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. The peptidoglycan ofScience translational medicine · 2025
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Implications of combinedFrontiers in immunology · 2023
    Article
  14. Article
  15. Review
  16. Article
  17. Article
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

7 authors at 2 institutions in 1 country.

Edgardo Guzman RiveraDivision of Rheumatology, Allergy and Immunology, Stony Brook University Renaissance School of Medicine, Stony Brook, NY, United States of America.
Asha PatnaikDivision of Rheumatology, Allergy and Immunology, Stony Brook University Renaissance School of Medicine, Stony Brook, NY, United States of America.
Joann SalveminiDepartment of Dermatology, Stony Brook University Renaissance School of Medicine, Stony Brook, NY, United States of America.
Sanjeev JainNew York Cancer and Blood Specialists, Patchogue, NY, United States of America.
Katherine LeeDepartment of Dermatology, Stony Brook University Renaissance School of Medicine, Stony Brook, NY, United States of America.
Daniel LozeauDepartment of Dermatology, Stony Brook University Renaissance School of Medicine, Stony Brook, NY, United States of America.
Qingping YaoDivision of Rheumatology, Allergy and Immunology, Stony Brook University Renaissance School of Medicine, Stony Brook, NY, United States of America. Electronic address: qingping.yao@stonybrookmedicine.edu.
Stony Brook University · USStony Brook School · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

COVID-19 infection activates the immune system to cause autoimmune and autoinflammatory diseases. We provide a comprehensive review of the relationship between SARS-CoV-2, NOD2 and ubiquitination. COVID-19 infection partly results from host inborn errors and genetic factors and can lead to autoinflammatory disease. The interaction between defective NOD2 and viral infection may trigger NOD2-associated disease. SARS-CoV-2 can alter UBA1 and abnormal ubiquitination leading to VEXAS syndrome. Both NOD2 and ubiquitination play important roles in controlling inflammatory process. Receptor interacting protein kinase 2 is a key component of the NOD2 activation pathway and becomes ubiquitinated to recruit downstream effector proteins. NOD2 mutations result in loss of ubiquitin binding and increase ligand-stimulated NOD2 signaling. During viral infection, mutations of either NOD2 or UBA1 genes or in combination can facilitate autoinflammatory disease. COVID-19 infection can cause autoinflammatory disease. There are reciprocal interactions between SARS-CoV-2, NOD2 and ubiquitination.

Indexed as

COVID-19Hereditary Autoinflammatory DiseasesHumansNod2 Signaling Adaptor ProteinSARS-CoV-2UbiquitinUbiquitinationNOD2 protein, humanNod2 Signaling Adaptor ProteinUbiquitinAutoinflammatory diseaseCOVID-19NOD2SARS-CoV-2UbiquitinationVEXAS syndromeYao syndrome

Identifiers

PMID35513305
PMCPMC9059341
OpenAlexW4225271743

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.