Evidence map›Paper›PMID 35437144›Full record

ArticleeLife2022

Multi-omics insights into host-viral response and pathogenesis in Crimean-Congo hemorrhagic fever viruses for novel therapeutic target.

Ujjwal Neogi, Nazif Elaldi, Sofia Appelberg, Anoop Ambikan, Emma Kennedy, Stuart Dowall, Binnur K Bagci, Soham Gupta, Jimmy E Rodriguez, Sara Svensson-Akusjärvi and 7 more

Abstract read
In one paragraph

Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
–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

24 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Effects ofViruses · 2025
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  8. Article
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  16. Article
  17. Systems-level temporal immune-metabolic profile in Crimean-Congo hemorrhagic fever virus infection.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  18. Role of Cx43 in iPSC-CM Damage Induced by Microwave Radiation.International journal of molecular sciences · 2023
    Article
  19. Article
  20. 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

17 authors.

Ujjwal Neogi *The Systems Virology Lab, Division of Clinical Microbiology, Department of Laboratory Medicine, Karolinska Institute, ANA Futura, Campus Flemingsberg, Stockholm, Sweden.ORCID 0000-0002-0844-3338
Nazif Elaldi *Department of Infectious Diseases and Clinical Microbiology, Medical Faculty, Cumhuriyet University, Sivas, Turkey.ORCID 0000-0002-9515-770X
Sofia AppelbergPublic Health Agency of Sweden, Solna, Sweden.
Anoop AmbikanThe Systems Virology Lab, Division of Clinical Microbiology, Department of Laboratory Medicine, Karolinska Institute, ANA Futura, Campus Flemingsberg, Stockholm, Sweden.ORCID 0000-0002-5221-9085
Emma KennedyPublic Health England, Porton Down, Salisbury, United Kingdom.
Stuart DowallPublic Health England, Porton Down, Salisbury, United Kingdom.
Binnur K BagciDepartment of Nutrition and Dietetics, Faculty of Health Sciences, Sivas Cumhuriyet University, Sivas, Turkey.
Soham GuptaThe Systems Virology Lab, Division of Clinical Microbiology, Department of Laboratory Medicine, Karolinska Institute, ANA Futura, Campus Flemingsberg, Stockholm, Sweden.
Jimmy E RodriguezDivision of Chemistry I, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.
Sara Svensson-AkusjärviThe Systems Virology Lab, Division of Clinical Microbiology, Department of Laboratory Medicine, Karolinska Institute, ANA Futura, Campus Flemingsberg, Stockholm, Sweden.
Vanessa MonteilDivision of Clinical Microbiology, Department of Laboratory Medicine, Karolinska Institute, ANA Futura, Campus Flemingsberg, Stockholm, Sweden.ORCID 0000-0002-2652-5695
Akos VegvariDivision of Chemistry I, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.
Rui BenfeitasNational Bioinformatics Infrastructure Sweden (NBIS), Science for Life Laboratory, Department of Biochemistry and Biophysics, Stockholm University, Stockholm, Sweden.ORCID 0000-0001-7972-0083
Akhil BanerjeaNational Institute of Immunology, Aruna Asaf Ali Marg, New Delhi, India.
Friedemann WeberInstitute for Virology, FB10-Veterinary Medicine, Justus-Liebig University, Giessen, Germany.
Roger HewsonPublic Health England, Porton Down, Salisbury, United Kingdom.
Ali MirazimiPublic Health Agency of Sweden, Solna, Sweden.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The pathogenesis and host-viral interactions of the Crimean-Congo hemorrhagic fever orthonairovirus (CCHFV) are convoluted and not well evaluated. Application of the multi-omics system biology approaches, including biological network analysis in elucidating the complex host-viral response, interrogates the viral pathogenesis. The present study aimed to fingerprint the system-level alterations during acute CCHFV-infection and the cellular immune responses during productive CCHFV-replication in vitro. We used system-wide network-based system biology analysis of peripheral blood mononuclear cells (PBMCs) from a longitudinal cohort of CCHF patients during the acute phase of infection and after one year of recovery (convalescent phase) followed by untargeted quantitative proteomics analysis of the most permissive CCHFV-infected Huh7 and SW13 cells. In the RNAseq analysis of the PBMCs, comparing the acute and convalescent-phase, we observed system-level host's metabolic reprogramming towards central carbon and energy metabolism (CCEM) with distinct upregulation of oxidative phosphorylation (OXPHOS) during CCHFV-infection. Upon application of network-based system biology methods, negative coordination of the biological signaling systems like FOXO/Notch axis and Akt/mTOR/HIF-1 signaling with metabolic pathways during CCHFV-infection were observed. The temporal quantitative proteomics in Huh7 showed a dynamic change in the CCEM over time and concordant with the cross-sectional proteomics in SW13 cells. By blocking the two key CCEM pathways, glycolysis and glutaminolysis, viral replication was inhibited in vitro. Activation of key interferon stimulating genes during infection suggested the role of type I and II interferon-mediated antiviral mechanisms both at the system level and during progressive replication.

Indexed as

Hemorrhagic Fever, CrimeanHemorrhagic Fever Virus, Crimean-CongoAntiviral AgentsCross-Sectional StudiesHumansInterferonsLeukocytes, MononuclearAntiviral AgentsInterferonsCCHFVimmunologyinfectious diseaseinflammationmetabolic controlmicrobiologytranscriptomicsviruses

Identifiers

PMID35437144
PMCPMC9018070

What OpenQuestion holds

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Registered trials

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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.