Evidence map›Paper›PMID 33867315›Full record

ReviewPulmonology

The immune response to SARS-CoV-2 and COVID-19 immunopathology - Current perspectives.

J L Boechat, I Chora, A Morais, L Delgado

Open access · diamondAbstract readReview
In one paragraph

Review in Pulmonology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 119 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
119citing papers in PubMed, 1 pooled it
11.4field-weighted citation impact, top 1% 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

119 citing papers in PubMed, 1 synthesis or guideline pooled it, 213 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. InflawellInflammopharmacology · 2022
    Trial
  5. Trial
  6. Neurodegenerative and Cognitive Consequences of Long COVID.International journal of molecular sciences · 2026
    Review
  7. Article
  8. Article
  9. COVID-19 Prophylactic Effect of Bromhexine Hydrochloride.Immunity, inflammation and disease · 2026
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Review
  19. Article
  20. Review

59 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

4 authors at 2 institutions in 2 countries.

J L BoechatClinical Immunology Service, Internal Medicine Department, Faculty of Medicine, Universidade Federal Fluminense, Niterói, RJ, Brazil; Basic and Clinical Immunology Unit, Department of Pathology, Faculty of Medicine, University of Porto, Portugal; Center for Health Technology and Services Research (CINTESIS), Faculty of Medicine, University of Porto, Portugal.
I ChoraInternal Medicine Service, Department of Medicine, Hospital Pedro Hispano, Unidade Local de Saúde de Matosinhos, Senhora da Hora, Portugal; Department of Medicine, Faculty of Medicine, University of Porto, Portugal.
A MoraisDepartment of Medicine, Faculty of Medicine, University of Porto, Portugal; Pulmonology Department, Centro Hospitalar e Universitario de Sao Joao, Porto, Portugal.
L DelgadoBasic and Clinical Immunology Unit, Department of Pathology, Faculty of Medicine, University of Porto, Portugal; Center for Health Technology and Services Research (CINTESIS), Faculty of Medicine, University of Porto, Portugal.
Universidade do Porto · PTUniversidade Federal Fluminense · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

SARS-CoV-2 is a new beta coronavirus, similar to SARS-CoV-1, that emerged at the end of 2019 in the Hubei province of China. It is responsible for coronavirus disease 2019 (COVID-19), which was declared a pandemic by the World Health Organization on March 11, 2020. The ability to gain quick control of the pandemic has been hampered by a lack of detailed knowledge about SARS-CoV-2-host interactions, mainly in relation to viral biology and host immune response. The rapid clinical course seen in COVID-19 indicates that infection control in asymptomatic patients or patients with mild disease is probably due to the innate immune response, as, considering that SARS-CoV-2 is new to humans, an effective adaptive response would not be expected to occur until approximately 2-3 weeks after contact with the virus. Antiviral innate immunity has humoral components (complement and coagulation-fibrinolysis systems, soluble proteins that recognize glycans on cell surface, interferons, chemokines, and naturally occurring antibodies) and cellular components (natural killer cells and other innate lymphocytes). Failure of this system would pave the way for uncontrolled viral replication in the airways and the mounting of an adaptive immune response, potentially amplified by an inflammatory cascade. Severe COVID-19 appears to be due not only to viral infection but also to a dysregulated immune and inflammatory response. In this paper, the authors review the most recent publications on the immunobiology of SARS-CoV-2, virus interactions with target cells, and host immune responses, and highlight possible associations between deficient innate and acquired immune responses and disease progression and mortality. Immunotherapeutic strategies targeting both the virus and dysfunctional immune responses are also addressed.

Indexed as

Adaptive ImmunityAdultAgedAntiviral AgentsCOVID-19Disease ProgressionHumansImmunity, InnateImmunotherapyInflammationLung Diseases, InterstitialMiddle AgedRespiration, ArtificialRespiratory Distress SyndromeSARS-CoV-2Severity of Illness IndexAntiviral AgentsCoronavirusCOVID-19ImmunopathologyImmunotherapyInnate immunitySARS-CoV-2

Identifiers

PMID33867315
PMCPMC8040543
OpenAlexW3155566633

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.