Evidence map›Paper›PMID 36075471›Full record

ArticleLife sciences2022

SARS-CoV-2 infection and replication kinetics in different human cell types: The role of autophagy, cellular metabolism and ACE2 expression.

Cynthia Silva Bartolomeo, Robertha Mariana Rodrigues Lemes, Rafael Leite Morais, Gabriela Cruz Pereria, Tamires Alves Nunes, Angelica Jardim Costa, Rui Monteiro de Barros Maciel, Carla Torres Braconi, Juliana Terzi Maricato, Luiz Mario Ramos Janini and 5 more

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Life sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.9field-weighted citation impact, top 5% 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

22 citing papers in PubMed, 40 citations in OpenAlex.

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  8. Interactions of SARS-CoV-2 with Human Target Cells-A Metabolic View.International journal of molecular sciences · 2024
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  17. Heliyon · 2023
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 2 institutions in 1 country.

Cynthia Silva BartolomeoDepartment of Physiological Sciences, Faculdade de Ciências Médicas da Santa Casa de São Paulo, São Paulo, SP, Brazil; Department of Biosciences, Universidade Federal de São Paulo, Santos, SP, Brazil.
Robertha Mariana Rodrigues LemesDepartment of Biological Sciences, Universidade Federal de São Paulo, Diadema, SP, Brazil; Laboratory of Molecular and Translational Endocrinology, Escola Paulista de Medicina, Universidade Federal de São Paulo, São Paulo, SP, Brazil.
Rafael Leite MoraisDepartment of Biophysics, Escola Paulista de Medicina, Universidade Federal de São Paulo, São Paulo, Brazil.
Gabriela Cruz PereriaDepartment of Biochemistry, Escola Paulista de Medicina, Universidade Federal de São Paulo, São Paulo, SP, Brazil.
Tamires Alves NunesDepartment of Biosciences, Universidade Federal de São Paulo, Santos, SP, Brazil.
Angelica Jardim CostaDepartment of Pharmacology, Escola Paulista de Medicina, Universidade Federal de São Paulo, São Paulo, SP, Brazil.
Rui Monteiro de Barros MacielDepartment of Biological Sciences, Universidade Federal de São Paulo, Diadema, SP, Brazil; Department of Medicine, Escola Paulista de Medicina, Universidade Federal de São Paulo, São Paulo, SP, Brazil.
Carla Torres BraconiDepartment of Microbiology Immunology and Parasitology, Escola Paulista de Medicina, Universidade Federal de São Paulo, São Paulo, SP, Brazil.
Juliana Terzi MaricatoDepartment of Microbiology Immunology and Parasitology, Escola Paulista de Medicina, Universidade Federal de São Paulo, São Paulo, SP, Brazil.
Luiz Mario Ramos JaniniDepartment of Microbiology Immunology and Parasitology, Escola Paulista de Medicina, Universidade Federal de São Paulo, São Paulo, SP, Brazil.
Liria Hiromi OkudaInstituto Biológico, Secretaria de Agricultura e Abastecimento, São Paulo, SP, Brazil.
Kil Sun LeeDepartment of Biochemistry, Escola Paulista de Medicina, Universidade Federal de São Paulo, São Paulo, SP, Brazil.
Carla Máximo PradoDepartment of Biosciences, Universidade Federal de São Paulo, Santos, SP, Brazil.
Rodrigo Portes UreshinoDepartment of Biological Sciences, Universidade Federal de São Paulo, Diadema, SP, Brazil; Laboratory of Molecular and Translational Endocrinology, Escola Paulista de Medicina, Universidade Federal de São Paulo, São Paulo, SP, Brazil.
Roberta Sessa StilhanoDepartment of Physiological Sciences, Faculdade de Ciências Médicas da Santa Casa de São Paulo, São Paulo, SP, Brazil. Electronic address: roberta.yamaguchi@fcmsantacasasp.edu.br.
Universidade Federal de São Paulo · BRInstituto Biológico · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsThis study evaluated SARS-CoV-2 replication in human cell lines derived from various tissues and investigated molecular mechanisms related to viral infection susceptibility and replication. MAIN

methodsSARS-CoV-2 replication in BEAS-2B and A549 (respiratory tract), HEK-293 T (kidney), HuH7 (liver), SH-SY5Y (brain), MCF7 (breast), Huvec (endothelial) and Caco-2 (intestine) was evaluated by RT-qPCR. Concomitantly, expression levels of ACE2 (Angiotensin Converting Enzyme) and TMPRSS2 were assessed through RT-qPCR and western blot. Proteins related to autophagy and mitochondrial metabolism were monitored in uninfected cells to characterize the cellular metabolism of each cell line. The effect of ACE2 overexpression on viral replication in pulmonary cells was also investigated. KEY

findingsOur data show that HuH7, Caco-2 and MCF7 presented a higher viral load compared to the other cell lines. The increased susceptibility to SARS-CoV-2 infection seems to be associated not only with the differential levels of proteins intrinsically related to energetic metabolism, such as ATP synthase, citrate synthase, COX and NDUFS2 but also with the considerably higher TMPRSS2 mRNA expression. The two least susceptible cell types, BEAS-2B and A549, showed drastically increased SARS-CoV-2 replication capacity when ACE2 was overexpressed. These modified cell lines are relevant for studying SARS-CoV-2 replication in vitro. SIGNIFICANCE: Our data not only reinforce that TMPRSS2 expression and cellular energy metabolism are important molecular mechanisms for SARS-CoV-2 infection and replication, but also indicate that HuH7, MCF7 and Caco-2 are suitable models for mechanistic studies of COVID-19. Moreover, pulmonary cells overexpressing ACE2 can be used to understand mechanisms associated with SARS-CoV-2 replication.

Indexed as

COVID-19NeuroblastomaAdenosine TriphosphateAngiotensin-Converting Enzyme 2AutophagyCaco-2 CellsCitrate (si)-SynthaseHEK293 CellsHumansPeptidyl-Dipeptidase ARNA, MessengerSARS-CoV-2Adenosine TriphosphateAngiotensin-Converting Enzyme 2Citrate (si)-SynthasePeptidyl-Dipeptidase ARNA, MessengerACE2AutophagyCell linesCOVID-19MitochondriaTMPRSS2

Identifiers

PMID36075471
PMCPMC9444585
OpenAlexW4294710591

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.