Evidence map›Paper›PMID 36421821›Full record

ArticleGenes2022

Anticipating the Next Chess Move: Blocking SARS-CoV-2 Replication and Simultaneously Disarming Viral Escape Mechanisms.

Samir Mansour Moraes Casseb, André Salim Khayat, Jorge Estefano Santana de Souza, Edivaldo Herculano Correa de Oliveira, Sidney Emanuel Batista Dos Santos, Pedro Fernando da Costa Vasconcelos, Paulo Pimentel de Assumpção

Open access · goldAbstract read
In one paragraph

Article in Genes, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.4field-weighted citation impact, top 39% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Article
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 3 institutions in 1 country.

Samir Mansour Moraes CassebOncology Research Center, Federal University of Pará, Belém 66073-000, Brazil.ORCID 0000-0002-7419-3381
André Salim KhayatOncology Research Center, Federal University of Pará, Belém 66073-000, Brazil.ORCID 0000-0002-3451-6369
Jorge Estefano Santana de SouzaBioinformatics Graduate Program, Metrópole Digital Institute, Federal University of Rio Grande do Norte Natal, Natal 59078-400, Brazil.
Edivaldo Herculano Correa de OliveiraOncology Research Center, Federal University of Pará, Belém 66073-000, Brazil.
Sidney Emanuel Batista Dos SantosOncology Research Center, Federal University of Pará, Belém 66073-000, Brazil.ORCID 0000-0002-8622-9417
Pedro Fernando da Costa VasconcelosDepartment of Pathology, Pará State University, Belém 66087-670, Brazil.ORCID 0000-0002-6603-5527
Paulo Pimentel de AssumpçãoOncology Research Center, Federal University of Pará, Belém 66073-000, Brazil.
Universidade Federal do Pará · BRUniversidade do Estado do Pará · BRUniversidade Federal do Rio Grande do Norte · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The COVID-19 pandemic initiated a race to determine the best measures to control the disease and to save as many people as possible. Efforts to implement social distancing, the use of masks, and massive vaccination programs turned out to be essential in reducing the devastating effects of the pandemic. Nevertheless, the high mutation rates of SARS-CoV-2 challenge the vaccination strategy and maintain the threat of new outbreaks due to the risk of infection surges and even lethal variations able to resist the effects of vaccines and upset the balance. Most of the new therapies tested against SARS-CoV-2 came from already available formulations developed to treat other diseases, so they were not specifically developed for SARS-CoV-2. In parallel, the knowledge produced regarding the molecular mechanisms involved in this disease was vast due to massive efforts worldwide. Taking advantage of such a vast molecular understanding of virus genomes and disease mechanisms, a targeted molecular therapy based on siRNA specifically developed to reach exclusive SARS-CoV-2 genomic sequences was tested in a non-transformed human cell model. Since coronavirus can escape from siRNA by producing siRNA inhibitors, a complex strategy to simultaneously strike both the viral infectious mechanism and the capability of evading siRNA therapy was developed. The combined administration of the chosen produced siRNA proved to be highly effective in successfully reducing viral load and keeping virus replication under control, even after many days of treatment, unlike the combinations of siRNAs lacking this anti-anti-siRNA capability. Additionally, the developed therapy did not harm the normal cells, which was demonstrated because, instead of testing the siRNA in nonhuman cells or in transformed human cells, a non-transformed human thyroid cell was specifically chosen for the experiment. The proposed siRNA combination could reduce the viral load and allow the cellular recovery, presenting a potential innovation for consideration as an additional strategy to counter or cope COVID-19.

Indexed as

COVID-19SARS-CoV-2Genome, ViralHumansPandemicsRNA, Small InterferingVirus ReplicationRNA, Small InterferingCOVID-19SARS-CoV-2siRNAtreatment

Identifiers

PMID36421821
PMCPMC9690012
OpenAlexW4309457217

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.