Evidence map›Paper›PMID 33337932›Full record

ReviewJournal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research2020

Role of Host Immune and Inflammatory Responses in COVID-19 Cases with Underlying Primary Immunodeficiency: A Review.

Benjamin M Liu, Harry R Hill

Open access · greenAbstract readReview
In one paragraph

Review in Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 2 pooled it
1.2field-weighted citation impact, top 11% 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

69 citing papers in PubMed, 2 syntheses or guidelines pooled it, 98 citations in OpenAlex.

  1. Pooled it
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  8. Clinical features and risk factors for severe macrolide-resistant mycoplasma pneumoniae pneumonia induced by 23 S rRNA A2063G mutation: a retrospective observational study.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2025
    Observational
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  10. Review
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  15. Clinical relevance of lung microbiota composition in critically ill children with acute lower respiratory tract infections: insights from a retrospective analysis of metagenomic sequencing.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2025
    Article
  16. Observational
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  19. Comparison of clinical and laboratory characteristics of COVID-19 and influenza in hospitalized children.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2024
    Article
  20. The impact of optimizing microbial diagnosis processes on clinical and healthcare economic outcomes in hospitalized patients with bloodstream infections.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2024
    Article

9 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Benjamin M LiuDepartment of Pathology, University of Utah School of Medicine, Salt Lake City, Utah, USA.
Harry R HillDepartment of Pathology, University of Utah School of Medicine, Salt Lake City, Utah, USA.
ARUP Laboratories (United States) · USUniversity of Utah · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Coronavirus disease 2019 (COVID-19) has spread rapidly and become a pandemic. Caused by a novel human coronavirus called severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), severe COVID-19 is characterized by cytokine storm syndromes due to innate immune activation. Primary immunodeficiency (PID) cases represent a special patient population whose impaired immune system might make them susceptible to severe infections, posing a higher risk to COVID-19, but this could also lead to suppressed inflammatory responses and cytokine storm. It remains an open question as to whether the impaired immune system constitutes a predisposing or protective factor for PID patients when facing SARS-CoV-2 infection. After literature review, it was found that, similar to other patient populations with different comorbidities, PID patients may be susceptible to SARS-CoV-2 infection. Their varied immune status, however, may lead to different disease severity and outcomes after SARS-CoV-2 infection. PID patients with deficiency in antiviral innate immune signaling [eg, Toll-like receptor (TLR)3, TLR7, or interferon regulatory factor 7 (IRF7)] or interferon signaling (IFNAR2) may be linked to severe COVID-19. Because of its anti-infection, anti-inflammatory, and immunomodulatory effects, routine intravenous immunoglobulin therapy may provide some protective effects to the PID patients.

Indexed as

Immune SystemInflammationComorbidityCOVID-19Disease SusceptibilityHumansImmunity, InnateImmunoglobulins, IntravenousInterferon Regulatory Factor-7PandemicsPrimary Immunodeficiency DiseasesReceptor, Interferon alpha-betaRiskToll-Like Receptor 3Toll-Like Receptor 7IFNAR2 protein, humanImmunoglobulins, IntravenousInterferon Regulatory Factor-7IRF7 protein, humanReceptor, Interferon alpha-betaTLR3 protein, humanTLR7 protein, humanToll-Like Receptor 3Toll-Like Receptor 7COVID-19cytokine release syndromeinnate immunityIVIGprimary immunodeficiencySARS-CoV-2

Identifiers

PMID33337932
PMCPMC7757688
OpenAlexW3111252009

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.