Evidence map›Paper›PMID 33124149›Full record

ReviewThe FEBS journal2021

The effects of aging on host resistance and disease tolerance to SARS-CoV-2 infection.

Darren Z L Mok, Candice Yuen Yue Chan, Eng Eong Ooi, Kuan Rong Chan

Open access · hybridAbstract readReview
In one paragraph

Review in The FEBS journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.2field-weighted citation impact, top 33% 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

11 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Clinical features of chronic fungal rhinosinusitis in Korean geriatric and non-geriatric patients.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2023
    Article
  7. Disease tolerance: a protective mechanism of lung infections.Frontiers in cellular and infection microbiology · 2023
    Review
  8. Review
  9. Article
  10. Article
  11. Review
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 3 institutions in 1 country.

Darren Z L MokEmerging Infectious Diseases Program, Duke-NUS Medical School, Singapore, Singapore.ORCID 0000-0002-4340-7535
Candice Yuen Yue ChanDepartment of Infectious Diseases, Singapore General Hospital, Singapore.
Eng Eong OoiEmerging Infectious Diseases Program, Duke-NUS Medical School, Singapore, Singapore.ORCID 0000-0002-0520-1544
Kuan Rong ChanEmerging Infectious Diseases Program, Duke-NUS Medical School, Singapore, Singapore.ORCID 0000-0002-2427-671X
Duke-NUS Medical School · SGSingapore General Hospital · SGSingHealth · SG

Funding

National Medical Research Council MOH-000135-00
6 · The paper itself

Abstract

The ongoing coronavirus disease 2019 (COVID-19) crisis caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has triggered a large-scale pandemic that is afflicting millions of individuals in over 200 countries. The clinical spectrum caused by SARS-CoV-2 infections can range from asymptomatic infection to mild undifferentiated febrile illness to severe respiratory disease with multiple complications. Elderly patients (aged 60 and above) with comorbidities such as cardiovascular diseases and diabetes mellitus appear to be at highest risk of a severe disease outcome. To protect against pulmonary immunopathology caused by SARS-CoV-2 infection, the host primarily depends on two distinct defense strategies: resistance and disease tolerance. Resistance is the ability of the host to suppress and eliminate incoming viruses. By contrast, disease tolerance refers to host responses that promote host health regardless of their impact on viral replication. Disruption of either resistance or disease tolerance mechanisms or both could underpin predisposition to elevated risk of severe disease during viral infection. Aging can disrupt host resistance and disease tolerance by compromising immune functions, weakening of the unfolded protein response, progressive mitochondrial dysfunction, and altering metabolic processes. A comprehensive understanding of the molecular mechanisms underlying declining host defense in elderly individuals could thus pave the way to provide new opportunities and approaches for the treatment of severe COVID-19.

Indexed as

AgedAgingCOVID-19Disease ResistanceHost-Pathogen InteractionsHumansImmune TolerancePandemicsSARS-CoV-2Virus ReplicationagingCOVID-19ER stressimmunometabolismimmunosenescenceresistanceSARS-CoV-2tolerance

Identifiers

PMID33124149
PMCPMC8518758
OpenAlexW3095252941

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.