Evidence map›Paper›PMID 33533523›Full record

ReviewCell biology international2021

Host-virus interaction and viral evasion.

Scheilla T Strumillo, Denis Kartavykh, Fábio F de Carvalho, Nicolly C Cruz, Ana C de Souza Teodoro, Ricardo Sobhie Diaz, Marli F Curcio

Open access · greenAbstract readReview
In one paragraph

Review in Cell biology international, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 7% 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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

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  19. Garcinone C inhibits pseudorabies virus replication through EGF/PI3K/Akt axis.Frontiers in cellular and infection microbiology · 2025
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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

7 authors at 2 institutions in 1 country.

Scheilla T StrumilloDepartment of Biochemistry, Laboratory of Cell Signaling, Federal University of São Paulo, São Paulo, Brazil.
Denis KartavykhDepartment of Medicine, Laboratory of Retrovirology, Federal University of São Paulo, São Paulo, Brazil.
Fábio F de CarvalhoDepartament of Educational Development, Getulio Vargas Foundation, São Paulo, Brazil.
Nicolly C CruzDepartment of Medicine, Laboratory of Retrovirology, Federal University of São Paulo, São Paulo, Brazil.ORCID https://orcid.org/0000-0002-7418-1540
Ana C de Souza TeodoroDepartment of Biochemistry, Laboratory of Cell Signaling, Federal University of São Paulo, São Paulo, Brazil.
Ricardo Sobhie DiazDepartment of Medicine, Laboratory of Retrovirology, Federal University of São Paulo, São Paulo, Brazil.ORCID https://orcid.org/0000-0002-8395-7304
Marli F CurcioDepartment of Medicine, Laboratory of Retrovirology, Federal University of São Paulo, São Paulo, Brazil.ORCID https://orcid.org/0000-0001-6476-4198
Universidade Federal de São Paulo · BRFundação Getulio Vargas · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

With each infectious pandemic or outbreak, the medical community feels the need to revisit basic concepts of immunology to understand and overcome the difficult times brought about by these infections. Regarding viruses, they have historically been responsible for many deaths, and such a peculiarity occurs because they are known to be obligate intracellular parasites that depend upon the host's cell machinery for their replication. Successful infection with the production of essential viral components requires constant viral evolution as a strategy to manipulate the cellular environment, including host internal factors, the host's nonspecific and adaptive immune responses to viruses, the metabolic and energetic state of the infected cell, and changes in the intracellular redox environment during the viral infection cycle. Based on this knowledge, it is fundamental to develop new therapeutic strategies for controlling viral dissemination, by means of antiviral therapies, vaccines, or antioxidants, or by targeting the inhibition or activation of cell signaling pathways or metabolic pathways that are altered during infection. The rapid recovery of altered cellular homeostasis during viral infection is still a major challenge. Here, we review the strategies by which viruses evade the host's immune response and potential tools used to develop more specific antiviral therapies to cure, control, or prevent viral diseases.

Indexed as

Immune EvasionAnimalsHumansImmunity, InnateMetabolic Networks and PathwaysVirus DiseasesVirusesVirus Physiological PhenomenaVirus Replicationcytokinesimmunityimmunologyinterleukinsoxidative stressviruses

Identifiers

PMID33533523
PMCPMC8014853
OpenAlexW3126398232

What Socratic 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 Socratic graph.