Evidence map›Paper›PMID 39470726›Full record

ArticleeLife2024

Longitudinal transcriptional changes reveal genes from the natural killer cell-mediated cytotoxicity pathway as critical players underlying COVID-19 progression.

Matias A Medina, Francisco Fuentes-Villalobos, Claudio Quevedo, Felipe Aguilera, Raul Riquelme, Maria Luisa Rioseco, Sebastian Barria, Yazmin Pinos, Mario Calvo, Ian Burbulis and 4 more

Abstract read
In one paragraph

Article in eLife, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Observational
  3. Article
  4. 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

14 authors.

Matias A MedinaFacultad de Medicina y Ciencia, Universidad San Sebastián, Puerto Montt, Chile.ORCID https://orcid.org/0000-0002-1905-6771
Francisco Fuentes-VillalobosDepartamento de Microbiología, Facultad de Ciencias Biológicas, Universidad de Concepción, Concepción, Chile.ORCID https://orcid.org/0000-0003-3120-0198
Claudio QuevedoDepartamento de Bioquímica y Biología Molecular, Facultad de Ciencias Biológicas, Universidad de Concepción, Concepción, Chile.
Felipe AguileraDepartamento de Bioquímica y Biología Molecular, Facultad de Ciencias Biológicas, Universidad de Concepción, Concepción, Chile.ORCID https://orcid.org/0000-0003-3235-931X
Raul RiquelmeFacultad de Medicina y Ciencia, Universidad San Sebastián, Puerto Montt, Chile.
Maria Luisa RiosecoFacultad de Medicina y Ciencia, Universidad San Sebastián, Puerto Montt, Chile.
Sebastian BarriaFacultad de Medicina y Ciencia, Universidad San Sebastián, Puerto Montt, Chile.
Yazmin PinosHospital Base San José, Osorno, Chile.
Mario CalvoInstituto de Medicina, Facultad de Medicina, Universidad Austral, Valdivia, Chile.
Ian BurbulisFacultad de Medicina y Ciencia, Universidad San Sebastián, Puerto Montt, Chile.
Camila KossackFacultad de Medicina y Ciencia, Universidad San Sebastián, Puerto Montt, Chile.ORCID https://orcid.org/0000-0002-3036-8813
Raymond A AlvarezDivision of Infectious Diseases, Department of Medicine, Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, United States.
Jose Luis GarridoFacultad de Medicina y Ciencia, Universidad San Sebastián, Puerto Montt, Chile.
Maria Ines BarriaFacultad de Medicina y Ciencia, Universidad San Sebastián, Puerto Montt, Chile.ORCID https://orcid.org/0000-0001-6225-5971

Funding

National Agency of Research and Development ATE220034National Agency of Research and Development Project COVID0422Universidad San Sebastian USS-FIN-23-PDOC-02
6 · The paper itself

Abstract

Patients present a wide range of clinical severities in response severe acute respiratory syndrome coronavirus 2 infection, but the underlying molecular and cellular reasons why clinical outcomes vary so greatly within the population remains unknown. Here, we report that negative clinical outcomes in severely ill patients were associated with divergent RNA transcriptome profiles in peripheral immune cells compared with mild cases during the first weeks after disease onset. Protein-protein interaction analysis indicated that early-responding cytotoxic natural killer cells were associated with an effective clearance of the virus and a less severe outcome. This innate immune response was associated with the activation of select cytokine-cytokine receptor pathways and robust Th1/Th2 cell differentiation profiles. In contrast, severely ill patients exhibited a dysregulation between innate and adaptive responses affiliated with divergent Th1/Th2 profiles and negative outcomes. This knowledge forms the basis of clinical triage that may be used to preemptively detect high-risk patients before life-threatening outcomes ensue.

Indexed as

COVID-19Killer Cells, NaturalSARS-CoV-2AdultAgedCytokinesDisease ProgressionFemaleHumansImmunity, InnateLongitudinal StudiesMaleMiddle AgedTranscriptomeCytokinesCOVID-19humaninfectious diseasemicrobiologyNKPBMC RNA-seq

Identifiers

PMID39470726
PMCPMC11521369

What OpenQuestion 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 OpenQuestion graph.