Evidence map›Paper›PMID 39457048›Full record

ReviewInternational journal of molecular sciences2024

Immunity and Coagulation in COVID-19.

Piotr P Avdonin, Maria S Blinova, Anastasia A Serkova, Lidia A Komleva, Pavel V Avdonin

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
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

9 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. COVID-19 Infection, Drugs, and Liver Injury.Journal of clinical medicine · 2025
    Review
  5. Article
  6. Article
  7. COVID-19: a vascular nightmare unfolding.Frontiers in immunology · 2025
    Review
  8. Article
  9. Brain histopathological changes caused by SARS-CoV-2 infection.Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologie
    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

5 authors.

Piotr P AvdoninKoltzov Institute of Developmental Biology RAS, ul. Vavilova, 26, 119334 Moscow, Russia.
Maria S BlinovaKoltzov Institute of Developmental Biology RAS, ul. Vavilova, 26, 119334 Moscow, Russia.
Anastasia A SerkovaKoltzov Institute of Developmental Biology RAS, ul. Vavilova, 26, 119334 Moscow, Russia.
Lidia A KomlevaKoltzov Institute of Developmental Biology RAS, ul. Vavilova, 26, 119334 Moscow, Russia.
Pavel V AvdoninKoltzov Institute of Developmental Biology RAS, ul. Vavilova, 26, 119334 Moscow, Russia.ORCID 0000-0002-4138-1589

Funding

Government program of basic research 0088-2024-0009Russian Science Foundation 22-15-00409
6 · The paper itself

Abstract

Discovered in late 2019, the SARS-CoV-2 coronavirus has caused the largest pandemic of the 21st century, claiming more than seven million lives. In most cases, the COVID-19 disease caused by the SARS-CoV-2 virus is relatively mild and affects only the upper respiratory tract; it most often manifests itself with fever, chills, cough, and sore throat, but also has less-common mild symptoms. In most cases, patients do not require hospitalization, and fully recover. However, in some cases, infection with the SARS-CoV-2 virus leads to the development of a severe form of COVID-19, which is characterized by the development of life-threatening complications affecting not only the lungs, but also other organs and systems. In particular, various forms of thrombotic complications are common among patients with a severe form of COVID-19. The mechanisms for the development of thrombotic complications in COVID-19 remain unclear. Accumulated data indicate that the pathogenesis of severe COVID-19 is based on disruptions in the functioning of various innate immune systems. The key role in the primary response to a viral infection is assigned to two systems. These are the pattern recognition receptors, primarily members of the toll-like receptor (TLR) family, and the complement system. Both systems are the first to engage in the fight against the virus and launch a whole range of mechanisms aimed at its rapid elimination. Normally, their joint activity leads to the destruction of the pathogen and recovery. However, disruptions in the functioning of these innate immune systems in COVID-19 can cause the development of an excessive inflammatory response that is dangerous for the body. In turn, excessive inflammation entails activation of and damage to the vascular endothelium, as well as the development of the hypercoagulable state observed in patients seriously ill with COVID-19. Activation of the endothelium and hypercoagulation lead to the development of thrombosis and, as a result, damage to organs and tissues. Immune-mediated thrombotic complications are termed "immunothrombosis". In this review, we discuss in detail the features of immunothrombosis associated with SARS-CoV-2 infection and its potential underlying mechanisms.

Indexed as

Blood CoagulationCOVID-19SARS-CoV-2ThrombosisHumansImmunity, InnatecoagulationcomplementCOVID-19immunothrombosisinflammationthrombotic microangiopathies

Identifiers

PMID39457048
PMCPMC11508857

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.