Evidence map›Paper›PMID 32485314›Full record

ArticleMedical hypotheses2020

Persistent SARS-CoV-2 infection and the risk for cancer.

Miguel Alpalhão, João Augusto Ferreira, Paulo Filipe

Open access · greenAbstract read
In one paragraph

Article in Medical hypotheses, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
0.7field-weighted citation impact, top 17% 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

24 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
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  7. Coronavirus disease 2019 and lung cancer: where are we?Exploration of targeted anti-tumor therapy · 2023
    Review
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  10. SARS-CoV2 Infection and Comorbidities, Role in Oncogenesis.Asian Pacific journal of cancer prevention : APJCP · 2022
    Article
  11. Article
  12. Review
  13. Article
  14. Review
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  16. SARS-CoV-2 infection and cancer: Evidence for and against a role of SARS-CoV-2 in cancer onset.BioEssays : news and reviews in molecular, cellular and developmental biology · 2021
    Review
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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

3 authors at 1 institution in 1 country.

Miguel AlpalhãoDermatology Department, Hospital de Santa Maria, Centro Hospitalar Universitário Lisboa Norte EPE, Lisbon, Portugal; Dermatology Universitary Clinic, Faculty of Medicine, University of Lisbon, Lisbon, Portugal; Dermatology Research Unit, iMM João Lobo Antunes, University of Lisbon, Lisbon, Portugal. Electronic address: migueldbalpalhao@campus.ul.pt.
João Augusto FerreiraDermatology Universitary Clinic, Faculty of Medicine, University of Lisbon, Lisbon, Portugal; Dermatology Research Unit, iMM João Lobo Antunes, University of Lisbon, Lisbon, Portugal.
Paulo FilipeDermatology Department, Hospital de Santa Maria, Centro Hospitalar Universitário Lisboa Norte EPE, Lisbon, Portugal; Dermatology Universitary Clinic, Faculty of Medicine, University of Lisbon, Lisbon, Portugal; Dermatology Research Unit, iMM João Lobo Antunes, University of Lisbon, Lisbon, Portugal.
University of Lisbon · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The current SARS-CoV-2 has put significant strain on healthcare services worldwide due to acute COVID-19. However, the potential long-term effects of this infection haven't been extensively discussed. We hypothesize that SARS-CoV-2 may be able to cause persistent infection in some individuals, and should this be the case, that in a few years we may see a rise in cancer incidence due to carcinogenic effects of this coronavirus. Non-retroviral RNA viruses such as Coronaviridae have been shown to cause persistent infection in hosts. Empirical evidence of viral genomic material shedding weeks after apparent clinical and laboratorial resolution of COVID-19 may be an indirect proof for persistent viral infection. Furthermore, tropism towards certain immune-privileged territories may facilitate immune evasion by this virus. Structural homology with SARS-CoV-1 indicates that SARS-CoV-2 may be able to directly impair pRb and p53, which are key gatekeepers with tumor suppressor functions. Additionally, COVID-19 features preeminent inflammatory response with marked oxidative stress, which acts as both as initiator and promotor of carcinogenesis. Should there be a carcinogenic risk associated with SARS-CoV-2, the implications for public health are plenty, as infected patients should be closely watched during long periods of follow-up. Additional investigation to establish or exclude the possibility for persistent infection is paramount to identify and prevent possible complications in the future.

Indexed as

BetacoronavirusAngiotensin-Converting Enzyme 2CarcinogenesisCoronavirus InfectionsCOVID-19HumansModels, BiologicalNeoplasmsOxidative StressPandemicsPeptidyl-Dipeptidase APneumonia, ViralReceptors, VirusRisk FactorsSARS-CoV-2ACE2 protein, humanAngiotensin-Converting Enzyme 2Peptidyl-Dipeptidase AReceptors, VirusCoronavirusInfectionsNeoplasmsPandemicsRisk

Identifiers

PMID32485314
PMCPMC7831646
OpenAlexW3031726837

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.