Evidence map›Paper›PMID 32360608›Full record

ReviewProgress in biophysics and molecular biology2020

Forecasting the timeframe of 2019-nCoV and human cells interaction with reverse engineering.

Ayesha Sohail, Alessandro Nutini

Open access · greenAbstract readReview
In one paragraph

Review in Progress in biophysics and molecular biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

12 citing papers in PubMed, 33 citations in OpenAlex.

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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

2 authors at 1 institution in 1 country.

Ayesha SohailDepartment of Mathematics, Comsats University Islamabad, Lahore Campus, Lahore, 54000, Pakistan. Electronic address: ayeshasohail81@gmail.com.
Alessandro NutiniCentro Studi Attività Motorie - Biomechanics Division, via di Tiglio 94 loc. Arancio, Lucca, 55100 Italy.
COMSATS University Islamabad · PK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In December 2019, an atypical pneumonia invaded the city of Wuhan, China, and the causative agent of this disease turned out to be a new coronavirus. In January 2020, the World Health Organization named the new coronavirus 2019-nCoV and subsequently it is referred to as SARS-CoV2 and the related disease as CoViD-19 (Lai et al., 2020). Very quickly, the epidemic led to a pandemic and it is now a worldwide emergency requiring the creation of new antiviral therapies and a related vaccine. The purpose of this article is to review and investigate further the molecular mechanism by which the SARS-CoV2 virus infection proceeds via the formation of a hetero-trimer between its protein S, the ACE2 receptor and the B0AT1 protein, which is the "entry receptor" for the infection process involving membrane fusion (Li et al., 2003). A reverse engineering process uses the formalism of the Hill function to represent the functions related to the dynamics of the biochemical interactions of the viral infection process. Then, using a logical evaluation of viral density that measures the rate at which the cells are hijacked by the virus (and they provide a place for the virus to replicate) and considering the "time delay" given by the interaction between cell and virus, the expected duration of the incubation period is predicted. The conclusion is that the density of the virus varies from the "exposure time" to the "interaction time" (virus-cells). This model can be used both to evaluate the infectious condition and to analyze the incubation period.

backgroundThe ongoing threat of the new coronavirus SARS-CoV2 pandemic is alarming and strategies for combating infection are highly desired. This RNA virus belongs to the β-coronavirus genus and is similar in some features to SARS-CoV. Currently, no vaccine or approved medical treatment is available. The complex dynamics of the rapid spread of this virus can be demonstrated with the aid of a computational framework.

methodsA mathematical model based on the principles of cell-virus interaction is developed in this manuscript. The amino acid sequence of S proein and its interaction with the ACE-2 protein is mimicked with the aid of Hill function. The mathematical model with delay is solved with the aid of numerical solvers and the parametric values are obtained with the help of MCMC algorithm.

resultsA delay differential equation model is developed to demonstrate the dynamics of target cells, infected cells and the SARS-CoV2. The important parameters and coefficients are demonstrated with the aid of numerical computations. The resulting thresholds and forecasting may prove to be useful tools for future experimental studies and control strategies.

conclusionsFrom the analysis, I is concluded that control strategy via delay is a promising technique and the role of Hill function formalism in control strategies can be better interpreted in an inexpensive manner with the aid of a theoretical framework.

Indexed as

Molecular Dynamics SimulationAmino Acid Transport Systems, NeutralAngiotensin-Converting Enzyme 2BetacoronavirusCell MembraneCell Membrane PermeabilityCoronavirus InfectionsCOVID-19HumansMembrane ProteinsPandemicsPeptidyl-Dipeptidase APneumonia, ViralProtein BindingReceptors, VirusRecombinant Fusion ProteinsACE2 protein, humanAmino Acid Transport Systems, NeutralAngiotensin-Converting Enzyme 2Membrane ProteinsPeptidyl-Dipeptidase AReceptors, VirusRecombinant Fusion ProteinsSLC6A19 protein, humanDynamical analysisKinetic modellingMCMC analysisMonoclonal antibodyNumerical simulationsSARS-CoV2

Identifiers

PMID32360608
PMCPMC7189847
OpenAlexW3022564109

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.