Evidence map›Paper›PMID 33463909›Full record

ArticlePhysiological reports2021

17β-estradiol reduces SARS-CoV-2 infection in vitro.

Robertha Mariana Rodrigues Lemes, Angelica Jardim Costa, Cynthia Silva Bartolomeo, Taysa Bervian Bassani, Michelle Sayuri Nishino, Gustavo Jose da Silva Pereira, Soraya Soubhi Smaili, Rui Monteiro de Barros Maciel, Carla Torres Braconi, Edgar Ferreira da Cruz and 6 more

Open access · goldAbstract read
In one paragraph

Article in Physiological reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.3field-weighted citation impact, top 6% 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

37 citing papers in PubMed, 53 citations in OpenAlex.

  1. Trial
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  3. Influence of Sex and 1,25α Dihydroxyvitamin DPathogens (Basel, Switzerland) · 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

16 authors at 2 institutions in 1 country.

Robertha Mariana Rodrigues LemesDepartment of Biological Sciences, Universidade Federal de São Paulo, Diadema, SP, Brazil.
Angelica Jardim CostaDepartment of Pharmacology, Escola Paulista de Medicina, Universidade Federal de São Paulo, São Paulo, SP, Brazil.
Cynthia Silva BartolomeoDepartment of Physiological Sciences, Faculdade de Ciências Médicas da Santa Casa de São Paulo, São Paulo, SP, Brazil.
Taysa Bervian BassaniDepartment of Biological Sciences, Universidade Federal de São Paulo, Diadema, SP, Brazil.
Michelle Sayuri NishinoDepartment of Biological Sciences, Universidade Federal de São Paulo, Diadema, SP, Brazil.
Gustavo Jose da Silva PereiraDepartment of Pharmacology, Escola Paulista de Medicina, Universidade Federal de São Paulo, São Paulo, SP, Brazil.
Soraya Soubhi SmailiDepartment of Pharmacology, Escola Paulista de Medicina, Universidade Federal de São Paulo, São Paulo, SP, Brazil.
Rui Monteiro de Barros MacielLaboratory of Molecular and Translational Endocrinology, 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.
Edgar Ferreira da CruzDepartment of Microbiology Immunology and Parasitology, Escola Paulista de Medicina, Universidade Federal de São Paulo, São Paulo, SP, Brazil.
Ana Lopez RamirezCambridge Institute for Medical Research, Cambridge, UK.
Juliana Terzi MaricattoDepartment 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.
Carla Máximo PradoDepartament of Biosciences, Universidade Federal de São Paulo, Santos, SP, Brazil.
Roberta Sessa StilhanoDepartment of Physiological Sciences, Faculdade de Ciências Médicas da Santa Casa de São Paulo, São Paulo, SP, Brazil.
Rodrigo Portes UreshinoDepartment of Biological Sciences, Universidade Federal de São Paulo, Diadema, SP, Brazil.ORCID https://orcid.org/0000-0003-3371-3376
Universidade Federal de São Paulo · BRFaculdade de Ciências Médicas da Santa Casa de São Paulo · BR

Funding

Conselho Nacional de Desenvolvimento Científico e Tecnológico 303035/2018-8Conselho Nacional de Desenvolvimento Científico e Tecnológico 405691/2018-1Coordenação de Aperfeiçoamento de Pessoal de Nível Superior Finance code 001FAP-FCMSCSP 2019/2021Fundação de Amparo à Pesquisa do Estado de São Paulo 2006/60402-1Fundação de Amparo à Pesquisa do Estado de São Paulo 2016/20796-2Fundação de Amparo à Pesquisa do Estado de São Paulo 2018/06088-0Fundação de Amparo à Pesquisa do Estado de São Paulo 2019/10922-9Fundação de Amparo à Pesquisa do Estado de São Paulo 2020/04709-8Fundação de Amparo à Pesquisa do Estado de São Paulo 2020/06153-7
6 · The paper itself

Abstract

The COVID-19 has originated from Wuhan, China, in December 2019 and has been affecting the public health system, society, and economy in an unheard-of manner. There is no specific treatment or vaccine available for COVID-19. Previous data showed that men are more affected than women by COVID-19, then we hypothesized whether sex hormones could be protecting the female organism against the infection. VERO E6 cells have been commonly used as in vitro model for SARS-CoV-2 infection. In our experimental approach, we have treated VERO E6 cells with 17β-estradiol to evaluate the modulation of SARS-CoV-2 infection in this cell line. Here we demonstrated that estrogen protein receptors ERα, ERβ, and GPER1 are expressed by VERO E6 cells and could be used to study the effects of this steroid hormone. Previous and 24-hours post-infection, cells treated with 17β-estradiol revealed a reduction in the viral load. Afterward, we found that SARS-CoV-2 infection per se results in ACE2 and TMPRSS2 increased gene expression in VERO E6-cell, which could be generating a cycle of virus infection in host cells. The estrogen treatment reduces the levels of the TMPRSS2, which are involved with SARS-CoV-2 infectiveness capacity, and hence, reducing the pathogenicity/genesis. These data suggest that estrogen could be a potential therapeutic target promoting cell protection against SARS-CoV-2. This opens new possibilities for further studies on 17β-estradiol in human cell lines infected by SARS-CoV-2 and at least in part, explain why men developed a more severe COVID-19 compared to women.

Indexed as

COVID-19 Drug TreatmentAngiotensin-Converting Enzyme 2AnimalsAntiviral AgentsChlorocebus aethiopsCOVID-19EstradiolHost-Pathogen InteractionsReceptors, VirusSARS-CoV-2Serine EndopeptidasesVero CellsAngiotensin-Converting Enzyme 2Antiviral AgentsEstradiolReceptors, VirusSerine Endopeptidases17β-estradiolCOVID-19estrogen receptorsgenderSARS-CoV-2VERO E6 cells

Identifiers

PMID33463909
PMCPMC7814496
OpenAlexW3125613216

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.